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2025, Volume 46, Issue 7
2025,
46(7):
1-9.
doi: 10.12259/j.issn.2095-610X.S20250701
Abstract:
Obesity has become a major global public health issue, and the situation in China is also becoming increasingly severe. Adipose tissue is categorized into white adipose tissue （WAT） and brown adipose tissue （BAT）, which regulates metabolic homeostasis by secreting various adipokines. Mitochondria, as the core organelles of energy metabolism, its dysfunction are closely related to obesity. In the state of obesity, mitochondrial dynamics imbalance, oxidative stress, and metabolic dysfunction can all lead to energy metabolism disorders and adipose tissue dysfunction. Moreover, mitochondrial dysfunction not only affects adipose tissue but also extends to multiple organs such as muscles and livers, thereby exacerbating obesity and related metabolic diseases. In recent years, although numerous therapeutic strategies targeting mitochondrial dysfunction have been actively explored, their clinical translation faces challenges. This review explores the association between mitochondrial dysfunction in adipose tissue and obesity, analyses its mechanism and existing treatment strategies, aiming to provide a new perspective for the diagnosis and treatment of obesity.
Obesity has become a major global public health issue, and the situation in China is also becoming increasingly severe. Adipose tissue is categorized into white adipose tissue （WAT） and brown adipose tissue （BAT）, which regulates metabolic homeostasis by secreting various adipokines. Mitochondria, as the core organelles of energy metabolism, its dysfunction are closely related to obesity. In the state of obesity, mitochondrial dynamics imbalance, oxidative stress, and metabolic dysfunction can all lead to energy metabolism disorders and adipose tissue dysfunction. Moreover, mitochondrial dysfunction not only affects adipose tissue but also extends to multiple organs such as muscles and livers, thereby exacerbating obesity and related metabolic diseases. In recent years, although numerous therapeutic strategies targeting mitochondrial dysfunction have been actively explored, their clinical translation faces challenges. This review explores the association between mitochondrial dysfunction in adipose tissue and obesity, analyses its mechanism and existing treatment strategies, aiming to provide a new perspective for the diagnosis and treatment of obesity.
2025,
46(7):
10-17.
doi: 10.12259/j.issn.2095-610X.S20250702
Abstract:
Objective To explore the role of ring finger protein 41 （RNF41） in the initiation and progression of cholangiocarcinoma. Methods The expression levels of RNF41 mRNA and protein in tumor tissues and adjacent normal tissues from 84 CHOL patients who underwent total surgical resection at the Second Affiliated Hospital of Kunming Medical University and Kunming Ganmei Hospital between January 2010 and December 2016 were analyzed using bioinformatics, Western blot, and immunohistochemistry. The TIMER 2.0 database was used to analyze the impact of RNF41 on the prognosis and survival of CHOL patients and the relationship between RNF41 and tumor clinical characteristics. RNF41 siRNA was transfected into HCC9810, RBE, and HUCCT1 cells. CCK-8, Edu, colony formation, and Western blot assays were conducted to evaluate the changes in proliferation of cholangiocarcinoma cells between the RNF41 knockdown group and the control group. Transwell assays and detection of EMT and migration markers were performed to assess changes in the invasion ability of cholangiocarcinoma cells between the RNF41 knockdown and control groups. Western blot was used to examine the effect of RNF41 knockdown on epithelial-mesenchymal transition in cholangiocarcinoma cells. Twelve BALB/c mice were randomly divided into two groups: a control group and an RNF41 knockdown group, with six mice in each group. Tumor formation assays, Western blot assays, and immunohistochemistry staining were carried out to investigate the effect of RNF41 knockdown on tumor growth in nude mice. Results Real-time quantitative fluorescence PCR analysis revealed that the expression level of RNF41 mRNA in cholangiocarcinoma tissues was significantly higher than that in the corresponding adjacent non-tumor tissues （P < 0.01）, and this trend was corroborated at the protein level by immunohistochemical staining. Using the TIMER 2.0 database, we further analyzed the correlation between RNF41 expression and clinicopathological features, including histological grade, tumor stage, lymph node metastasis, and patient survival. The results indicated that elevated RNF41 expression was significantly associated with advanced histological grade and lymph node metastasis in cholangiocarcinoma （P < 0.01）. Survival analysis demonstrated that high RNF41 expression was closely linked to poor prognosis in patients with cholangiocarcinoma （CHOL）. Functional assays, including CCK-8, EdU incorporation, and colony formation, showed that RNF41 knockdown significantly inhibited the proliferation of cholangiocarcinoma cells compared with the control group. Western blot analysis revealed that, following RNF41 silencing, the expression of the epithelial-mesenchymal transition （EMT） marker E-cadherin was markedly upregulated, whereas the levels of mesenchymal markers N-cadherin and MMP9 were significantly reduced （P < 0.05）. These findings were consistent with the results obtained from in vitro experiments （P < 0.01）. Moreover, in vivo studies showed that RNF41 knockdown suppressed subcutaneous tumor formation in nude mice （P < 0.05）. Conclusion RNF41 plays a critical role in promoting the occurrence and progression of cholangiocarcinoma and is closely associated with adverse clinicopathological features and poor prognosis in patients. The knockdown of RNF41 effectively suppresses the proliferation, invasion, epithelial-mesenchymal transition （EMT）, and tumorigenicity of cholangiocarcinoma cells.
2025,
46(7):
18-25.
doi: 10.12259/j.issn.2095-610X.S20250703
Abstract:
Objective To investigate the mechanism by which Scutellaria barbata D. Don water extract （SBW） inhibits lung metastasis of breast cancer by regulating the immune microenvironment. Methods A mouse model of lung metastasis was established using 4T1 breast cancer cells. Mice were divided into a control group （n = 6） and an SBW treatment group （n = 6）. The effect of SBW on tumor growth was assessed by measuring the volume of the primary tumor, and the inhibitory effect on lung metastasis was evaluated by observing the number and area of metastatic nodules in lung tissue using H&E staining. Flow cytometry was used to analyze changes in the composition of immune cells in the tumor, peripheral blood, and lung tissue. Results Compared with the control group, the SBW treatment group inhibited the growth of the primary tumor （P < 0.01） and reduced the number and area of lung metastatic nodules （P < 0.01）. Flow cytometry analysis showed that after SBW treatment, the numbers of CD86+ macrophages （P < 0.001） and polymorphonuclear myeloid-derived suppressor cells （PMN-MDSCs） （P < 0.05） in the tumor tissue were increased. In lung tissue, the numbers of CD86+ macrophages, natural killer T （NKT） cells, natural killer （NK） cells, and PMN-MDSCs were also elevated （P < 0.05）. Meanwhile, the numbers of regulatory T cells （Tregs） （P < 0.05）, CD206+ macrophages （P < 0.01）, and monocytic myeloid-derived suppressor cells （M-MDSCs） （P < 0.05） in both tumor and lung tissues were decreased. Conclusion SBW inhibits the breast cancer growth and lung metastasis by regulating the recruitment and distribution of immune cells in the tumor, peripheral blood, and lung tissue, thereby enhancing anti-tumor immune responses and reducing immune suppression.
2025,
46(7):
26-37.
doi: 10.12259/j.issn.2095-610X.S20250704
Abstract:
Objective To explore the regulatory mechanism of NFE2L2/KEAP1 in alveolar bone repair induced by periodontitis. Methods A rat periodontitis model was established and divided into four groups: Control group （n = 6）; Periodontitis model group （n = 6）; Periodontitis + lentivirus empty vector group （n = 6）; Periodontitis + NFE2L2 overexpression plasmid group （n = 6）. Histopathological changes in each group were observed using HE staining. TRAP staining was used to detect osteoclast positivity, while ELISA was employed to measure inflammatory cytokine levels in tissues. Immunofluorescence and qPCR were used to detect NFE2L2 expression, and western blot was used to assess the expression of osteogenic proteins ALPL2, RUNX2, and COL1. Primary periodontal ligament cells （hPDLCs） were cultured, and cells were transfected to overexpress NFE2L2 and KEAP1. The cells were divided into six groups: Normal group; Model group; pcDNA-NC group; pcDNA-NFE2L2 group; pc-NFE2L2 + pcDNA-NC group; pc-NFE2L2 + pcDNA-KEAP1 group. A cellular model was established, and the morphology of primary hPDLCs was observed under a microscope. Cell proliferation was assessed using CCK-8. Osteogenic mineralization was observed using alizarin red staining, and western blot was used to detect osteogenic proteins and autophagy markers. Cell migration was observed using a scratch assay. Results （1） After model induction, redness, swelling of the gums, extensive inflammatory infiltration, and alveolar bone resorption were observed, confirming successful model establishment.Partial tissue recovery occurred after NFE2L2 overexpression via lentivirus. （2） After model induction, osteoclast positivity increased, confirming successful model establishment. Overexpression of NFE2L2 reduced osteoclast positivity （P < 0.001）. （3） After model induction, levels of IL-1β, IL-10, and TNF-α were significantly higher than in the normal group （P < 0.05）, confirming successful model establishment. Transfection with NFE2L2 lentivirus reduced inflammatory cytokine levels （P < 0.0001 ）. After model induction, osteogenic protein expression decreased compared to the normal group, but overexpression of NFE2L2 increased osteogenic protein expression （P < 0.05）. （5） LPS treatment significantly reduced cell viability, while NFE2L2 overexpression enhanced it （P < 0.0001 ）. （6） LPS treatment reduced calcified nodules, while NFE2L2 overexpression increased them. Addition of pcDNA-KEAP1 reduced mineralized nodules. （7） LPS treatment decreased osteogenic protein expression, while NFE2L2 overexpression increased it. However, addition of pcDNA-KEAP1 reduced osteogenic protein expression （P < 0.05）. （8） LPS treatment reduced cell migration, whereas NFE2L2 overexpression enhanced it （P < 0.0001 ）. （9） Expression of autophagy markers decreased after LPS treatment, but increased after transfection with NFE2L2 plasmid. However, addition of pcDNA-KEAP1 reduced the expression of autophagy markers （P < 0.05）. Conclusion This study identified the regulatory role of NFE2L2/KEAP1 in periodontitis, providing a scientific basis for the treatment of periodontitis.
2025,
46(7):
38-45.
doi: 10.12259/j.issn.2095-610X.S20250705
Abstract:
Objective To investigate the effect of ligustrazine on spinal cord repair from the perspective of macrophage autophagy and its molecular mechanism in a rat model. Methods A rat model of spinal cord injury was established using Allen's method. Successful modeling was indicated by hindlimb spasm, tail twisting, and Basso, Beattie, and Bresnahan （BBB） score of 0. The rats were divided into 4 groups: sham-operation group, model group, low-dose ligustrazine group, and high-dose ligustrazine group, with 10 rats in each group. The low-dose and high-dose ligustrazine groups were administered ligustrazine （150 mg/kg and 200 mg/kg, respectively） via intraperitoneal injection, while the normal and model groups received an equal volume of normal saline once daily for 28 days. At different time points after surgery, the hindlimb motor function of the rats was assessed using the BBB scale. Hematoxylin-eosin （HE） and Nissl staining were used to observe the histopathological changes in the spinal cord tissue and the morphology of neurons. Enzyme-linked immunosorbent assay （ELISA） was employed to detect the expression levels of superoxide dismutase （SOD） and malondialdehyde （MDA） in the spinal cord tissue. TUNEL staining was used to evaluate the apoptosis status of spinal cord neurons. Protein levels of LC3 I, LC3 II, Bax, and Bcl-2 in the spinal cord tissue were detected by Western Blot. Electron microscopy was used to observe the formation of autophagosomes in spinal cord macrophages, and immunofluorescence was used to detect the protein expression of LC3 II in spinal cord macrophages. Results Compared with the sham-operation group, the model group exhibited impaired hindlimb function and spinal cord tissue morphology （P < 0.05）, along with decreased levels of SOD, apoptosis, LC3 II/Ⅰ, Bcl-2 protein expression, autophagosome number in macrophages, and LC3 II protein expression, as well as increased levels of MDA, Bax, and Bax/Bcl-2 protein expression （P < 0.05）. Compared with the model group, both the low-dose and high-dose ligustrazine groups showed improved hindlimb function and spinal cord tissue morphology （P < 0.05）, with increased levels of SOD, apoptosis, LC3 II/Ⅰ, Bcl-2 protein expression, autophagosome number in macrophages, and LC3 II protein expression, as well as decreased levels of MDA, Bax, and Bax/Bcl-2 protein expression （P < 0.05）. The intervention effect of ligustrazine was dose-dependent. Conclusion Ligustrazine can effectively repair spinal cord injury in rats, and its molecular mechanism may be related to the activation of autophagy in spinal cord macrophages and the inhibition of neuronal apoptosis.
2025,
46(7):
46-53.
doi: 10.12259/j.issn.2095-610X.S20250706
Abstract:
Objective To investigate the expression of EIF5A1 in intrahepatic cholangiocarcinoma cell lines and human hepatobiliary duct epithelia, and its effect on the proliferation, migration and invasion ability and Wnt/β-Catenin signaling pathway in HUCCT1 cells . Methods Western blot was used to detect the basal expression level of EIF5A1 in intrahepatic cholangiocarcinoma cell lines and human intrahepatic cholangiocarcinoma epithelial cells. Transient transfection of siRNA was used to silence the expression of EIF5A1 in intrahepatic cholangiocarcinoma cell HUCCT1. The experimental groups were divided into blank control group (Con), siRNA1 group, and siRNA2 group. The most effective siRNA was screened by Western blot. The effects of EIF5A1 silencing on the proliferation, migration and invasion ability of HUCCT1 cells were detected by CCK-8, EdU cell proliferation assay and Transwell assay. The effect of EIF5A1 silencing on the Wnt/β-Catenin signaling pathway in HUCCT1 cells was detected by Western blot. Results The results of CCK-8 and EdU cell proliferation experiments showed that the proliferation ability of HUCCT1 cells decreased after EIF5A1 silencing （P < 0.05）, and Transwell migration and invasion experiments showed that the migration and invasion ability of Hucct1 cells decreased after EIF5A1 silencing （P < 0.05）. Western blot analysis revealed decreased expression of β-Catenin, Cyclin D1, MMP-2 and Survivin in Wnt/β-Catenin signaling pathway after EIF5A1 silencing （P < 0.05）. Conclusion EIF5A1 may promote the proliferation, migration and invasion of intrahepatic bile duct cancer cells through Wnt/β-Catenin signaling pathway.
2025,
46(7):
54-64.
doi: 10.12259/j.issn.2095-610X.S20250707
Abstract:
Objective To investigate the role of exosomal microRNA （miRNA） miR-210-3p in chemoresistance and stem cell property formation in cervical cancer, and to elucidate its underlying mechanism through targeting of F-box protein 31 （FBXO31）. Methods Exosomes were isolated from cisplatin-sensitive HeLa cells and cisplatin-resistant HeLa/DDP cells via ultracentrifugation, and their uptake by HeLa/DDP cells was verified using the PKH26 red fluorescent labeling method. HeLa cells were transfected with NC inhibitor, miR-210-3p inhibitor alone, or in combination with si-NC and si-FBXO31. After 24 hours of transfection, exosomes were extracted and co-cultured with HeLa/DDP cells for 48 hours. Consequently, HeLa/DDP cells were divided into five groups: the Ctrl group （PBS blank control）, the NC inhibitor group, the miR-210-3p inhibitor group, the miR-210-3p inhibitor+si-NC group and the miR-210-3p inhibitor+si-FBXO31 group. RT-qPCR was used to measure miR-210-3p and FBXO31 expression levels. The half-maximal inhibitory concentration （IC50） of cisplatin was determined using the MTT assay. Stem cell properties were assessed via tumor sphere formation assays. Western blot analysis was performed to detect the protein expression of FBXO31 and stem cell markers （e.g., SOX2, OCT4, NANOG）. The targeting relationship between miR-210-3p and FBXO31 was validated using dual-luciferase reporter assays. The effect of exosomal miR-210-3p on the metastasis of cervical cancer in vivo was evaluated by nude mice xenograft tumor. Resuts Compared with human normal cervical epithelial cells （HCeEpiC）, miR-210-3p expression was significantly upregulated in cervical cancer cell lines （HeLa, HT3, C33A, and CaSki）, while FBXO31 expression was significantly downregulated （P < 0.05）. HeLa/DDP cells （cisplatin-resistant） exhibited significantly higher miR-210-3p expression levels and IC50 values for cisplatin compared with parental HeLa cells （P < 0.05）, and HeLa exosomes were efficiently taken up by HeLa/DDP cells. Compared with the NC inhibitor groupThe miR-210-3p inhibitor group showed significantly reduced expression levels of miR-210-3p, OCT4, SOX2, and NANOG, as well as a significantly lower IC50 （P < 0.05）, while FBXO31 expression was significantly increased （P < 0.05）. Compared with the miR-210-3p inhibitor + si-NC group, the miR-210-3p inhibitor + si-FBXO31 group exhibited significantly decreased FBXO31 expression （P < 0.05） and increased IC50, Oct-4, SOX2, and NANOG expression （P < 0.05）. Compared with the control group and the empty vector group, the tumor weight and volume were significantly lower in the miR-210-3p than in the control and empty vector groups （P < 0.05）. Conclusion Exosomal miR-210-3p promotes chemoresistance to DDP and enhances stem cell-like properties in CC cells by directly targeting and inhibiting FBXO31.
2025,
46(7):
65-73.
doi: 10.12259/j.issn.2095-610X.S20250708
Abstract:
Objective To investigate the expression of serum microRNA-29b （miR-29b）, microRNA-199a （miR-199a）, and microRNA-19a-3p （miR-19a-3p） in patients with acute cerebral infarction （ACI） and their relationship with disease severity and prognosis. Methods （1） Rats were randomly divided into a control group （Control group） and a model group （Model group）, with 6 rats in each group. ACI was induced in the model group using the modified Longa suture method; the expression levels of miR-29b, miR-199a, miR-19a-3p in rat serum and brain tissue were detected and analyzed. （2）A total of 106 ACI patients diagnosed at Tangshan People's Hospital from June 2023 to June 2024 were enrolled as the study group, and 108 healthy individuals who underwent physical check-ups at the same hospital during the same period were chosen as the control group. According to the NIHSS evaluation results, the study group patients were assigned into mild （42 cases）, moderate （34 cases）, and severe （30 cases） groups. Based on the mRS evaluation results, the patients were assigned into good prognosis （68 cases） and poor prognosis （38 cases） groups. Real-time fluorescence quantitative PCR was applied to measure the expression levels of serum miR-29b, miR-199a, and miR-19a-3p. Pearson correlation analyzed the correlation between serum miR-29b, miR-199a, miR-19a-3p levels and NIHSS score and mRS score in ACI patients. The risk factors for poor prognosis in ACI patients were analyzed using multivariate logistic regression. ROC curves were used to analyze the predictive value of serum miR-29b, miR-199a, miR-19a-3p levels and NHISS scores in poor prognosis of ACI patients. Results （1） Compared with the Control group, the levels of miR-199a and miR-19a-3p in the serum and brain tissue of the Model group rats were significantly increased, while the level of miR-29b was significantly decreased （P < 0.05）; （2） Compared with the control group, as the severity of ACI patients gradually increased, the levels of serum miR-199a and miR-19a-3p unusually increased in the mild, moderate, and severe groups, while the level of miR-29b was significantly decreased （P < 0.05）. The NHISS score, miR-199a and miR-19a-3p levels in the poor prognosis group were significantly higher than those in the good prognosis group, while miR-29b was significantly lower than that in the good prognosis group（P < 0.05）. The levels of serum miR-199a and miR-19a-3p were positively correlated with NIHSS score; the level of miR-29b was negatively correlated with NIHSS score （P < 0.05）. Elevated serum miR-199a and miR-19a-3p levels and increased NHISS score were independent risk factors for poor prognosis in ACI patients, and elevated serum miR-29b levels were protective factors for poor prognosis in ACI patients （P < 0.05）. The combined prediction of poor prognosis in ACI patients using serum miR-29b, miR-199a, miR-19a-3p levels and NHISS scores yielded an ACI of 0.988, which was superior to individual predictions （Z = 2.878, 3.551, 3.300, 3.452, P < 0.05）. Conclusion The serum expression levels of miR-199a and miR-19a-3p were significantly up-regulated, while miR-29b levels significantly down-regulated, which were related to the disease severity and prognosis. The the combination of the three miRNAs had certain value in predicting the poor prognosis of patients. MiR-29b, miR-199a, and miR-19a-3p can be used as important predictors to evaluate the progression and prognosis of ACI patients.
2025,
46(7):
74-83.
doi: 10.12259/j.issn.2095-610X.S20250709
Abstract:
Objective To investigate the effects of BMSCs treatment on neuropathic pain in rats with SCI and explore the underlying mechanism. Methods The rats were randomly divided into the following groups (n=15 per group): sham-operated (sham) group, spinal cord injury model (SCI) group, SCI + BMSCs group, and SCI + BMSCs + LY294002 group. An SCI model was established using Sprague-Dawley rats, followed by intraspinal administration of BMSCs and the PI3K inhibitor LY294002 to the injured spinal cord of SCI rats. The BBB score, pMWT, and pTWL values under thermal stimulation were measured. Hematoxylin-eosin staining was used to observe pathological changes in the injured spinal cord of rats. The effects of BMSCs transplantation on SCI rats were explored through hematoxylin-eosin staining, immunofluorescence staining, ELISA, and Western Blot experiments. RSCN were induced using LPS and co-cultured with BMSCs and their exosomes. The effects of BMSCs and their exosomes on RSCN were investigated through Annexin V-FITC/PI kit, ELISA, and Western Blot assays. Results The SCI model was considered successfully established when the following criteria were met on post-operative day 5: BBB locomotor score ≤5, accompanied by a BBB score <10 on day 20, along with histopathological evidence of spinal cord tissue loosening, extensive vacuolation, and neuronal atrophy observed via HE staining. Compared with the sham group, the SCI group exhibited significantly lower BBB scores, pMWT, and pTWL values (P < 0.001). Concurrently, increased immunofluorescence intensity of IBA1, elevated levels of pro-inflammatory cytokines, and pain-related factors were detected in the spinal cord (P < 0.001). Furthermore, activation of the PI3K/AKT signaling pathway was significantly suppressed. BMSCs transplantation protected SCI rats by activating the PI3K/AKT pathway （P < 0.001）. BMSC-mediated spinal cord repair was attenuated by LY294002 administration. LPS-induced RSCNs showed increased apoptosis and pro-inflammatory cytokine release （P < 0.001）. Co-culture with MSCs or BMSCs-derived exosomes activated the PI3K/AKT signaling pathway, thereby reducing LPS-induced apoptosis and proinflammatory cytokine production （P < 0.05）. Conclusion BMSCs activate the PI3K/AKT signaling pathway in neurons through exosomes, suppressing the levels of TNF-α, SP, NE, and 5-HT, and promoting functional recovery in SCI rats.
Cyclin O Promotes the Proliferation and Metastasis of Cervical Cancer Cells by Regulating Glycolysis
2025,
46(7):
84-91.
doi: 10.12259/j.issn.2095-610X.S20250710
Abstract:
Objective To investigate the expression of Cyclin O （CCNO） in cervical cancer and its molecular mechanism in the progression of cervical cancer. Methods The pathological sections of 60 patients with cervical cancer in the Department of Oncology and Gynecology of the First Affiliated Hospital of Bengbu Medical University from January 2018 to December 2023 were collected, and the expression of CCNO in cervical cancer was detected by immunohistochemistry. The cells were divided into Vector group, CCNO group, siNC group and siCCNO group by transfection technology. CCK-8 assay and colony formation assay were used to evaluate the ability of CCNO to affect cell proliferation. Transwell assay and wound healing assay were used to evaluate the effect of CCNO on cell invasion and migration. Glycolysis assay and Western blot assay were used to evaluate the effect and mechanism of CCNO on glycolysis of cervical cancer cells. Results The results of immunohistochemistry and WB showed that CCNO was highly expressed in cervical cancer （P < 0.001）. Overexpression of CCNO promoted the proliferation, invasion, migration and glycolysis of cervical cancer cells （P < 0.05）, whereas the opposite effect inhibited the proliferation, invasion, migration and glycolysis of cervical cancer cells （P < 0.05）. Bioinformatics analysis and WB results showed that CCNO overexpression may regulate the occurrence of cervical cancer by activating the PI3K/AKT signaling pathway （P < 0.05）. Conclusion Cyclin O may promote the proliferation and metastasis of cervical cancer cells by regulating glycolysis.
2025,
46(7):
92-100.
doi: 10.12259/j.issn.2095-610X.S20250711
Abstract:
Objective To comprehensively assess the predictive value of C-reactive protein （CRP）/D-dimer （D-D） and albumin/fibrinogen （FAR） in predicting major adverse cardiovascular events （MACE） after percutaneous coronary intervention （PCI） in patients with coronary heart disease （CHD） and to construct a nomogram model for predicting post-procedural MACE in CHD patients. Methods A retrospective study was conducted on 201 CHD patients who underwent PCI at the First Affiliated Hospital of Kunming Medical University between June 2022 and March 2025. These patients were divided into MACE group （n = 77） and non-MACE group （n = 124） based on whether MACE occurred or not. 84 CHD patients from another medical center were also collected as the validation set. The expression levels of CRP/D-D and FAR were compared between the two groups; independent predictors of postoperative MACE in CHD patients were screened by univariate and multivariate logistic regression analyses; the predictive value of CRP/D-D and FAR for the occurrence of postoperative MACE in CHD patients was assessed using ROC curves; A nomogram model was established integrating indicators such as CRP/D-D and FAR, and internal and external validations of the nomogram model were conducted using ROC curves, calibration curves, and decision curve analysis （DCA） curves. Results Compared with CHD patients in the non-MACE group, CRP/D-D and FAR levels were significantly higher in the MACE group （P < 0.05）. Multivariate analysis showed that age, NTproBNP, WBC, CRP/D-D, and FAR were independent risk factors for postoperative MACE in CHD patients （P < 0.05）. ROC curve analysis indicated that the AUC predicted by CRP/D-D combined with FAR was higher than that of CRP/D-D alone （Z = 3.473, P < 0.001）, and FAR alone（Z = 2.812, P < 0.05） . The Nomogram model constructed based on the aforementioned factors was validated internally and externally, and the results showed that the Nomogram model had good calibration, excellent discriminative ability, and reliable clinical utility, accurately predicting the risk of postoperative MACE. Conclusion The CRP/D-D ratio and FAR, as emerging composite biomarkers, showed significant predictive ability in predicting the risk of MACE after PCI in patients with CHD, providing a new reliable tool for clinical risk stratification.
2025,
46(7):
101-109.
doi: 10.12259/j.issn.2095-610X.S20250712
Abstract:
Objective To investigate the correlation between the benign and malignant pulmonary nodules and serum inflammatory factors, tumor markers, and imaging features. Methods A total of 209 patients with pulmonary nodules who underwent lung puncture biopsy at the Third People's Hospital of Kunming from January 2023 to January 2024 were enrolled. Based on pathological results, the patients were divided into benign pulmonary nodules group （n=106） and malignant pulmonary nodules group （n=103）. General data and clinical indicators of all subjects were collected, and differences in various indicators between the two groups were analyzed. Results In terms of Serum inflammatory factors: there were statistically significant differences in LYMPH, NLR, LMR, IL-2, IL-6, IL-17, IFN-γ, HsCRP, SAA, and PCT between the two groups （P < 0.05）, while no significant differences were found in WBC, NETU, MONO, PLT, SII, IL-5, IFN-α, IL-1β, IL-10, IL-8, and IL-12P70 （P > 0.05）. Regarding Serum tumor markers: there were statistically significant differences in CEA, CA125, CA199, CYFRA21-1, ProGRP, and NSE between the two groups （P < 0.05）, whereas no significant differences were found in TSGF, AFP, and CA153 （P > 0.05）. In terms of Imaging features: there were statistically significant differences in the number, diameter, boundary, fissure sign, spiculated sign, and pleural retraction sign of nodules between the two groups （P < 0.05）, while no significant differences were found in nodular calcification, nodule density, and location （P > 0.05）. Binary logistic regression analysis （backward-Wald conditional method） identified patient age, fissure sign, CEA, NSE, ProGRP, and IL-6 were independent risk factors for malignant pulmonary nodules （P < 0.05）. The combined diagnostic model of these indicators for predicting malignant pulmonary nodules had an AUC of 0.965 （P < 0.05）. Conclusion Malignant pulmonary nodules are more likely in older patients with lobulation on imaging and elevated serum levels of NSE, ProGRP, IL-6, and CEA. Combined detection of these indicators can predict the nature of pulmonary nodules, guiding early diagnosis of malignant nodules.
2025,
46(7):
110-117.
doi: 10.12259/j.issn.2095-610X.S20250713
Abstract:
objective To investigate the prognostic value of plasma ADAMTS13 in patients with heart failure complicated with type 2 diabetes mellitus （T2DM）. Methods Clinical data were collected from adult patients with acute decompensated heart failure admitted to the Second People's Hospital of Yulin City from January 2019 to December 2020, with a total of 278 cases included. The level of ADAMTS13 was measured using an ELISA kit, and patients were divided into three groups based on the third quartile of ADAMTS13 : T1<9.9 μg/L group （n = 92）, T2 ≥ 10.0-18.5 μg/L group （n = 93）, and T3 ≥ 18.5 μg/L group （n = 93）. The primary outcome was defined as the composite end point of all-cause mortality's or heart failure readmission. Secondary outcomes included all-cause mortality and heart failure readmission. Results Compared with the patients in the highest third quartile of ADAMTS13, the number of T2DM cases, body mass index, uric acid, fasting blood glucose, HbA1c and hs-CRP levels in the patients with the lowest third quartile of ADAMTS13 increased significantly （P < 0.05）. The absolute risks of main outcome, all-cause death and hospitalization of heart failure were higher in T2DM patients than in non-T2DM patients （χ2 = 12.028, 8.725, 9.023, all P = 0.000）. The differences in heart failure rate among patients with different ADAMTS13 levels were statistically significant （χ2 = 9.384, P = 0.002）. Every doubling of ADAMTS13 was related to a decreased risk of the main outcomes in HF patients with T2DM （HR=0.69, 95%CI=0.61～0.79）, all-cause mortality （HR=0.59, 95%CI=0.47～0.74） and heart failure readmission （HR=0.75, 95%CI=0.65～0.87）. Conclusion ADAMTS13 is an independent biomarker for risk stratification in HF, especially in patients with T2DM.
2025,
46(7):
118-124.
doi: 10.12259/j.issn.2095-610X.S20250714
Abstract:
Objective To explore the expression of serum lipocalin-2 （LCN2） and latent transforming growth factor-β binding protein 2 （LTBP2） in ovarian cancer patients and their relationship with clinicopathological features and prognosis. Methods A total of 108 ovarian cancer patients treated in Baoji Hospital Affiliated to Xi'an Medical College from February 2020 to December 2021 were included in the ovarian cancer group. Another 108 patients with benign ovarian lesions during the same period were included and labeled as the lesion group, and 108 healthy female volunteers undergoing physical examination were assigned to the control group. ELISA method was used to detect serum LCN2 and LTBP2 levels. The relationship between serum LCN2 and LTBP2 levels and prognosis survival rate in ovarian cancer patients was analyzed using the Kaplan-Meier method. Multivariate Cox regression analysis was performed to identify the risk factors affecting the prognosis of ovarian cancer patients. Results Serum LCN2 and LTBP2 levels increased in the control group, lesion group, and ovarian cancer group in sequence （P < 0.05）. Among patients with high expression of serum LCN2 and LTBP2, the proportions of FIGO stage III-IV, tumor maximum diameter > 3 cm, and postoperative lymph node metastasis were higher than those of FIGO stages I-II, tumor maximum diameter ≤ 3 cm, and non lymph node metastasis （P < 0.05）. The median survival time of ovarian cancer patients with high serum LCN2 and LTBP2 expression was lower than that of patients with low expression （Log-rank χ2=5.367、6.305, P < 0.05）. The survival rate of patients with FIGO stage III～IV, maximum tumor diameter > 3 cm, postoperative lymph node metastasis, LCN2 and LTBP2 high expression was lower than that of patients with FIGO stage I～II, tumor maximum diameter ≤ 3 cm, no postoperative lymph node metastasis, and low LCN2 and LTBP2 expression （P < 0.05）. FIGO stages III-IV, maximum tumor diameter > 3 cm, postoperative lymph node metastasis, high LCN2, and high LTBP2 were independent risk factors affecting the 3-year survival rate of ovarian cancer patients （P < 0.05）. Conclusion Serum LCN2 and LTBP2 are upregulated in ovarian cancer patients, and are closely related to FIGO staging, tumor maximum diameter, and postoperative lymph node metastasis. They are important factors affecting prognosis and may serve as biomarkers for evaluating prognosis.
2025,
46(7):
125-130.
doi: 10.12259/j.issn.2095-610X.S20250715
Abstract:
Objective To investigate the relationship between the expression of platelet autophagy related factors and peritoneal metastasis of gastric cancer. Methods The data of 360 patients with gastric cancer who underwent surgery in Hunan Provincial People’ s Hospital from January 2021 to May 2023 were reviewed. Patients were divided into non-peritoneal metastasis group (n = 322) and peritoneal metastasis group (n = 38) according to whether peritoneal metastasis occurred or not. The following information was collected: patient's personal information （i.e. age, sex, body mass index） and tumor characteristics （i.e. location, size, pathological type, histopathological differentiation, lymphatic infiltration）. Platelets were collected from all subjects, and the levels of autophagy-associated protein 7（ATG7）, benzalkonium chloride 1（BECN1）, microtubule-associated protein 1 light chain 3（LC3） and sequestosome 1（p62） were measured by enzyme-linked immunosorbent assay （ELISA）. Results Among the 360 patients included, peritoneal metastasis was detected in 38 cases. Compared with the non-peritoneal metastasis group, the peritoneal metastasis group exhibited decreased BMI（P < 0.05）, while the tumor size, non-ulcerative tumor, number of lymph node metastasis, infiltration depth, number of cases of lymphatic invasion, platelet count, platelet LC3-II level, platelet ATG7 level and CEA level were increased （P < 0.05）. Multivariate logistic regression analysis showed that BMI （OR = 1.094）, lymphatic invasion （OR = 2.658）, and LC3-II （OR = 3.793） and ATG7（OR = 2.010） were independent influencing factors for peritoneal metastasis in patients with gastric cancer （P < 0.05）. LC3-II > 2.59ng/ml had the highest ability to predict peritoneal metastasis in patients with gastric cancer （AUC = 0.932）, followed by ATG7（AUC = 0.916）. Conclusions Elevated levels of platelet LC3-Ⅱ and ATG7 are independently related to peritoneal metastasis in patients with gastric cancer, and can be used to predict the occurrence of peritoneal metastasis, which is helpful to guide individualized treatment.
2025,
46(7):
131-138.
doi: 10.12259/j.issn.2095-610X.S20250716
Abstract:
Objective To investigate the interactive effects of diabetes and lipid abnormalities on the treatment efficacy of rheumatoid arthritis （RA） and their predictive significance, providing a basis for individualized treatment of RA patients with metabolic disorders. Methods A total of 180 RA patients who visited the hospital between June 2022 and June 2023 were selected as research subjects. Based on whether patients had diabetes and dyslipidemia, they were divided into Group A （RA only, n = 45）, Group B （RA with diabetes, n = 45）, Group C （RA with dyslipidemia, n = 45）, and Group D （RA with both diabetes and dyslipidemia, n = 45）. All patients received conventional anti-rheumatic treatment according to the 2018 Chinese Rheumatoid Arthritis Diagnosis and Treatment Guidelines. Patients in Group B and D were additionally treated with metformin for blood glucose control, while patients in Group C and D received statins for lipid regulation. Treatment efficacy was assessed after 3 months of treatment. The Observed indicators included American College of Rheumatology （ACR） 20/50/70 response rates, Disease Activity Score （DAS28）, C-reactive protein （CRP）, erythrocyte sedimentation rate （ESR）, glycated hemoglobin （HbA1c）, fasting plasma glucose （FPG）, total cholesterol （TC）, triglycerides （TG）, low-density lipoprotein cholesterol （LDL-C）, and high-density lipoprotein cholesterol （HDL-C）. Multivariate logistic regression analysis was used to evaluate the impact of blood glucose and lipid levels on RA treatment efficacy. Additive and multiplicative models were constructed to evaluate the interaction between HbA1c and HDL-C. Results After treatment, Group A showed significantly higher ACR20/50 response rates than the other three groups, and also showed a higher trend in ACR70 response rate. Group D had the lowest response rates across all criteria （P < 0.05）. Group D also exhibited significantly higher levels of DAS28, CRP, and ESR than the other three groups, while Group A had the lowest levels （P < 0.05）. Baseline HbA1c level, baseline HDL-C level and baseline DAS28 scores are independent influencing factors for ACR20 response （P < 0.05）. Comparison of additive and multiplicative models suggested that the effects of HbA1c and HDL-C on ACR20 response might be independent of each other （P = 0.652）. Conclusion Diabetes and dyslipidemia have significant negative impacts on RA treatment efficacy, but their interaction is not significant. For RA patients with metabolic disorders, it is important to actively control blood glucose and regulate lipid levels while undergoing anti-rheumatic treatment to improve therapeutic outcomes. Baseline HbA1c and HDL-C levels can serve as important predictors for RA treatment response.
2025,
46(7):
139-145.
doi: 10.12259/j.issn.2095-610X.S20250717
Abstract:
Objective To investigate the clinical efficacy of intravaginal CO2 fractional laser combined with interferon in treating persistent high-risk HPV infection of the cervix and its impact on vaginal microecology. Methods A total of 211 patients with persistent high-risk HPV infection of the cervix who visited Kunming Maternal and Child Health Care Hospital from June 2022 to July 2024 were selected and randomly divided into a follow-up （blank control） group （n = 70）, an interferon treatment group （n = 70）, and a combined treatment group （n = 71）. The follow-up group received regular follow-ups. The interferon treatment group was treated with recombinant human interferon α-2b, and the combined treatment group received a combination of CO2 matrix laser and interferon treatment. The total effective rate, levels of inflammatory factors, and vaginal microecological recovery were compared among the three groups at 3 and 6 months after treatment. Results Overall efficacy: The overall efficacy rates of the combined treatment group at 3 months and 6 months were 73.24% and 81.69%, respectively, significantly higher than those of the interferon group （47.14% and 60.00%） and the blank control group （11.43% and 18.57%） （all P < 0.001）. Inflammatory factors: Post-treatment levels of IL-1 and TNF-α in the combined treatment group were significantly lower than those in the other two groups （P < 0.001）. Vaginal microbiota: The combined treatment group had a significantly higher rate of normal PH （84.51%） and normal lactobacillus levels（92.96%） compared to the other two groups （P < 0.001）. Conclusion CO2 lattice laser combined with interferon can effectively eliminate HPV, improve inflammation and vaginal microenvironment, and demonstrates superior efficacy to monotherapy, with good safety.
2025,
46(7):
146-154.
doi: 10.12259/j.issn.2095-610X.S20250718
Abstract:
Objective To explore the relationship between serum Interleukin-27 （IL-27）, Cystatin C （CysC）, and Glyceraldehyde-3-phosphate dehydrogenase （GAPDH） antibodies and the severity of disease in children with Neuromyelitis optica spectrum disorder （NMOSD）, as well as their impact on prognosis. Methods A total of 102 children with NMOSD admitted to Kunming Children's Hospital from July 2019 to July 2023 were selected, along with 102 healthy during the same period. Serum levels of IL-27, CysC, and GAPDH antibodies were compared between children with NMOSD and healthy children. The levels of serum IL-27, CysC, and GAPDH antibodies were compared among children with varying disease severity. The correlations between serum IL-27, CysC, GAPDH antibodies and disease condition, cerebrospinal fluid markers were analyzed. And 102 children with NMOSD received individualized treatment and were followed up for 1 year. The prognosis was evaluated based on disease relapse, and patients were divided into recurrence group and non-recurrence group. The clinical data, serum IL-27, CysC, and GAPDH antibody levels were compared between the two groups. the impact of serum IL-27, CysC, and GAPDH antibodies on disease recurrence was analyzed, and the predictive value of serum IL-27, CysC, and GAPDH antibodies for disease recurrence was evaluated. Results Children with NMOSD had lower levels of serum IL-27 and CysC and higher levels of GAPDH antibodies than healthy children （P < 0.05）. Serum IL-27 and CysC levels were negatively correlated with Aquaporin 4 （AQP4）-IgG antibody positivity, the number of spinal cord-involved segments, Expanded disability status scale （EDSS） scores, cerebrospinal fluid protein content, and white blood cell count. In contrast GAPDH antibodies were positively correlated with these parameters （P < 0.05）. After 1-year follow-up, 2 cases were lost to follow-up, 21 cases relapsed, and 79 cases did not, which were included in the relapse group and non-relapse group, respectively. There were significant differences in the number of spinal cord-involved segments, EDSS scores, and cerebrospinal fluid protein content between the relapse group and non-relapse group （P < 0.05）. The levels of serum IL-27 and CysC were lower and the levels of GAPDH antibodies were higher in the relapse group than the non-relapse group （P < 0.05）. Serum IL-27, CysC, and GAPDH antibodies were significantly associated with disease relapse （P < 0.05）. The Area under the curve （AUC） values for predicting disease recurrence in children with NMOSD based on serum IL-27, CysC, and GAPDH antibodies were 0.748, 0.791, and 0.747, respectively, with optimal cutoff values of 38.77 pg/mL, 0.79 mg/L, and 55.81 pg/mL, respectively. The combined prediction of disease relapse using these three markers had an AUC of 0.900, which was superior to individual prediction values （Z = 2.215, 2.137, 2.220, P = 0.024, 0.033, 0.023）. Conclusion The levels of serum IL-27, CysC, and GAPDH antibodies are significantly correlated with the disease severity and prognosis in children with NMOSD, and can effectively predict the risk of disease recurrence. Combined detection provides more reliable predictive value.
2025,
46(7):
155-162.
doi: 10.12259/j.issn.2095-610X.S20250719
Abstract:
Objective To investigate the predictive value of multimodal magnetic resonance imaging （MRI） in the progression of transient ischemic attack （TIA） patients. Methods A retrospective study was conducted on 103 TIA patients admitted to the First Affiliated Hospital of Kangda College, Nanjing Medical University （Lianyungang First People’ s Hospital） from September 2021 to December 2023. These patients were divided into the TIA group （34 cases） and the ACI group （69 cases） based on whether they progressed to acute cerebral infarction （ACI）. All patients underwent multimodal magnetic resonance examinations after admission. The imaging results of the cranial T1WI, T2WI, DWI, TOF-MRA, high-resolution magnetic resonance imaging, and magnetic resonance imaging perfusion-weighted imaging [plaque burden, stenosis degree, enhancement index, pial collateral grading, cerebral blood flow （CBF）, cerebral blood volume （CBV）, mean transit time （MTT）, and time to peak （TTP）] were compared between the two groups. The correlation between multimodal MRI findings and ACI risk, as well as their predictive value for ACI, were analyzed. Additionally, multimodal MRI results were compared among patients with different degrees of neurological deficits and different prognoses. Results The ACI group exhibited higher plaque load, stenosis degree, enhancement index, MTT and TTP, worse pIA collateral grade, and lower CBF and CBV compared to the TIA group （P < 0.05）. Logistic regression analysis revealed that plaque burden, stenosis degree, enhancement index, MTT, and TTP were associated risk factors for disease progression in TIA patients （OR value > 1, P < 0.001）, while pial collateral grade, CBF, and CBV were associated protective factors for disease progression in TIA patients （OR value < 1, P < 0.001）. ROC curve showed that the AUC of ACI predicted by combination of plaque load, stenosis degree, enhancement index, MTT, TTP, pia collateral grade, CBF and CBV was 0.914 （95%CI: 0.842～0.960）, which was greater than that of pia collateral grade alone（Z = 0.314, P < 0.05）.Bootstrap internal validation showed that the joint prediction results were well aligned with the ideal curve, indicating that the predicted incidence of ACI was consistent with the actual incidence. The plaque load, stenosis degree, enhancement index, MTT and TTP of patients with severe neurological deficits were higher than those with mild to moderate deficits, and CBF and CBV were lower than those of mild to moderate patients （P < 0.05）. The plaque load, stenosis degree, enhancement index, MTT and TTP of patients with poor prognosis were highe, and CBF and CBV were lower than those of with good prognosis （P < 0.05）. Conclusion Multimodal MRI has certain predictive value for the disease progression in TIA patients, providing a reference for clinical assessment of the condition and prognosis prediction, and helping to formulate targeted follow-up intervention plans.
2025,
46(7):
163-174.
doi: 10.12259/j.issn.2095-610X.S20250720
Abstract:
Metabolic dysfunction-associated steatotic liver disease （MASLD） is a chronic liver condition intricately linked to metabolic abnormalities such as obesity, type 2 diabetes, dyslipidemia, and hypertension. The global prevalence of MASLD continues to rise, posing a significant public health challenge.The pathogenesis of MASLD is multifactorial, with the "multiple-hit" hypothesis suggesting that hepatic lipid accumulation, insulin resistance, oxidative stress, gut microbiota dysbiosis, and genetic factors collectively drive disease progression. Currently, clinical management primarily relies on lifestyle interventions; however, there is a lack of targeted pharmacological interventions, and there is an urgent need to investigate novel adjunctive therapeutic strategies. In recent years, probiotics have demonstrated potential value in MASLD treatment due to their capacity to modulate gut microbiota, enhance insulin sensitivity, and reduce liver inflammation. This review systematically examines the pathogenesis of MASLD and the limitations of existing therapeutic approaches, synthesizing the latest evidence of probiotics-assisted therapy for MASLD from the perspectives of animal studies and clinical trials.By analyzing the target mechanisms and molecular pathways of different strains （e.g., Bifidobacterium, Lactobacillus）, this review explores the translational potential of probiotics in MASLD treatment, aiming to provide a theoretical foundation and future research directions.
Metabolic dysfunction-associated steatotic liver disease （MASLD） is a chronic liver condition intricately linked to metabolic abnormalities such as obesity, type 2 diabetes, dyslipidemia, and hypertension. The global prevalence of MASLD continues to rise, posing a significant public health challenge.The pathogenesis of MASLD is multifactorial, with the "multiple-hit" hypothesis suggesting that hepatic lipid accumulation, insulin resistance, oxidative stress, gut microbiota dysbiosis, and genetic factors collectively drive disease progression. Currently, clinical management primarily relies on lifestyle interventions; however, there is a lack of targeted pharmacological interventions, and there is an urgent need to investigate novel adjunctive therapeutic strategies. In recent years, probiotics have demonstrated potential value in MASLD treatment due to their capacity to modulate gut microbiota, enhance insulin sensitivity, and reduce liver inflammation. This review systematically examines the pathogenesis of MASLD and the limitations of existing therapeutic approaches, synthesizing the latest evidence of probiotics-assisted therapy for MASLD from the perspectives of animal studies and clinical trials.By analyzing the target mechanisms and molecular pathways of different strains （e.g., Bifidobacterium, Lactobacillus）, this review explores the translational potential of probiotics in MASLD treatment, aiming to provide a theoretical foundation and future research directions.
2025,
46(7):
175-180.
doi: 10.12259/j.issn.2095-610X.S20250721
Abstract:
Objective To explore the application effect of a BOPPPS-based blended teaching model in adult nursing course. Methods A total of 188 undergraduate nursing students from the school of Nursing, Kunming Medical university, in the class of 2021 were enrolled as research subjects and grouped by classes（97 students in the control group and 91 students in the experimental group）. During the teaching process, the control group and the experimental group respectively adopted the traditional teaching model and the blended teaching model based on BOPPPS. The teaching effect was evaluated through the pre-assessment and post-assessment theoretical scores, learning engagement, independent learning ability and teacher quality of the two groups of students. Results The differences between the pre-assessment and post-assessment theoretical scores of the two groups were statistically significant, and the scores of the experimental group were 86.80（78.73, 94.09）, which were higher than those of the control group 79.45（69.39, 87.97）（P < 0.05）. There were also statistically significant differences in the scores of learning engagement and independent learning ability between the two groups after teaching （P < 0.05）. Conclusion The blended teaching model based on BOPPPS used in the teaching of adult nursing for undergraduate nursing students can effectively improve the teaching effect, which is conducive to improving their learning engagement and stimulating students' learning autonomy.
