Effects of Decursin on Myocardial Fibrosis Following Myocardial Infarction

Aikebaier Mirenuer; Wei FANG; Rujuan ZHAO; Sujie GUO; Chuning FENG; Ying YANG; Ke YANG

Article Contents

Article Navigation > Journal of Kunming Medical University > 2026 > Accepted Manuscript

Aikebaier Mirenuer, Wei FANG, Rujuan ZHAO, Sujie GUO, Chuning FENG, Ying YANG, Ke YANG. Effects of Decursin on Myocardial Fibrosis Following Myocardial Infarction[J]. Journal of Kunming Medical University.

Citation:

Aikebaier Mirenuer, Wei FANG, Rujuan ZHAO, Sujie GUO, Chuning FENG, Ying YANG, Ke YANG. Effects of Decursin on Myocardial Fibrosis Following Myocardial Infarction[J]. Journal of Kunming Medical University.

Citation:

PDF( 2807 KB)

Effects of Decursin on Myocardial Fibrosis Following Myocardial Infarction

1.
Department of Cardiovascular Medicine，Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine，Shanghai 200025
2.
Department of Cardiovascular Medicine，PLA Navy 905 Hospital，Shanghai 200052
3.
School of Pharmacy，Yunnan University，Department of Biology and Medicine，Kunming Yunnan 6505044
4.
Department of Nephrology，Yueyang Hospital of Integrated Traditional Chinese and Western Medicine Affiliated to Shanghai University of Traditional Chinese Medicine，Shanghai 200437
5.
Shanghai Jiao Tong University School of Medicine，Shanghai 200025，China

Received Date: 2026-03-12

Abstract

Abstract

Objective To investigate the effects of Decursin （DEC） on myocardial fibrosis after myocardial infarction in mice and its regulatory mechanism underlying the activation of cardiac fibroblasts （CFs）. Methods C57BL/6 mice were subjected to ligation of the left anterior descending coronary artery to establish a mouse myocardial infarction model. The mice were randomly divided into three groups （n = 5 per group）: sham operation group （Sham）, myocardial infarction model group （MI）, and decursin treatment group （DEC）. DEC was administered by intragastric gavage. For 28 days post-surgery, cardiac function was evaluated by echocardiography; histopathological changes and the degree of myocardial fibrosis were assessed by immunohistochemistry. The migratory capacity of cardiac fibroblasts was determined by wound-healing assay; the proliferation of cardiac fibroblasts was detected by EdU assay. The expression levels of key proteins related to myocardial fibrosis signaling pathways were measured by Western blot （WB）. Results Echocardiographic assessment revealed that compared with the MI group, the DEC treatment group exhibited significantly increased left ventricular ejection fraction （LVEF, increased by 25%, P < 0.001）, left ventricular fractional shortening （LVFS, increased by 16%, P < 0.001）, and mitral valve E/A ratio （MV E/A, P < 0.001）. Immunohistochemical results showed that the MI group presented increased myocardial interstitial collagen deposition and enlarged fibrotic area （P < 0.001）, whereas DEC intervention markedly attenuated the fibrotic process （P < 0.01）. In vitro experiments demonstrated that DEC significantly inhibited the proliferation （P < 0.01） and migration （P < 0.05） of cardiac fibroblasts, downregulated the expression of fibronectin （P < 0.05）, α-SMA, collagen I and other proteins （P < 0.01）, and suppressed the activation of cardiac fibroblasts. Conclusion Decursin can improve cardiac function and attenuate myocardial fibrosis after myocardial infarction, and its mechanism may be associated with the PI3K/AKT signaling pathway.
- Decursin,
- Myocardial infarction,
- Myocardial fibrosis,
- Fibroblasts,
- PI3K/AKT signaling pathway

FullText(HTML)

References(19)

References

[1]	Mensah G A, Fuster V, Murray C J L, et al. Global burden of cardiovascular diseases and risks, 1990-2022[J]. J Am Coll Cardiol, 2023, 82(25): 2350-2473. doi: 10.1016/j.jacc.2023.11.007
[2]	Sharma A, Vidusha K, Suresh H, et al. Global awareness of myocardial infarction symptoms in general population: A systematic review and meta-analysis[J]. Korean Circ J, 2021, 51(12): 983. doi: 10.4070/kcj.2021.0100
[3]	Frangogiannis N G. Cardiac fibrosis[J]. Cardiovasc Res, 2021, 117(6): 1450-1488. doi: 10.1093/cvr/cvaa324
[4]	Pesce M, Duda G N, Forte G, et al. Cardiac fibroblasts and mechanosensation in heart development, health and disease[J]. Nat Rev Cardiol, 2023, 20(5): 309-324. doi: 10.1038/s41569-022-00799-2
[5]	Maruyama K, Imanaka-Yoshida K. The pathogenesis of cardiac fibrosis: A review of recent progress[J]. Int J Mol Sci, 2022, 23(5): 2617. doi: 10.3390/ijms23052617
[6]	Plikus M V, Wang X, Sinha S, et al. Fibroblasts: Origins, definitions, and functions in health and disease[J]. Cell, 2021, 184(15): 3852-3872. doi: 10.1016/j.cell.2021.06.024
[7]	Ghazal R, Wang M, Liu D, et al. Cardiac fibrosis in the multi-omics era: Implications for heart failure[J]. Circ Res, 2025, 136(7): 773-802. doi: 10.1161/CIRCRESAHA.124.325402
[8]	Muralikrishnan A, Sekar M, Kumarasamy V, et al. Chemistry, pharmacology and therapeutic potential of decursin: A promising natural lead for new drug discovery and development[J]. Drug Des Dev Ther, 2024, 18: 3741-3763. doi: 10.2147/DDDT.S476279
[9]	Ge Y, Yoon S H, Jang H, et al. Decursin promotes HIF-1α proteasomal degradation and immune responses in hypoxic tumour microenvironment[J]. Phytomedicine, 2020, 78: 153318. doi: 10.1016/j.phymed.2020.153318
[10]	Son D B, Choi W, Kim M, et al. Decursin alleviates mechanical allodynia in a paclitaxel-induced neuropathic pain mouse model[J]. Cells, 2021, 10(3): 547. doi: 10.3390/cells10030547
[11]	Choi Y J, Kim D H, Kim S J, et al. Decursin attenuates hepatic fibrogenesis through interrupting TGF-beta-mediated NAD(P)H oxidase activation and Smad signaling in vivo and in vitro[J]. Life Sci, 2014, 108(2): 94-103. doi: 10.1016/j.lfs.2014.05.012
[12]	Que R, Cao M, Dai Y, et al. Decursin ameliorates carbon-tetrachloride-induced liver fibrosis by facilitating ferroptosis of hepatic stellate cells[J]. Biochem Cell Biol, 2022, 100(5): 378-386. doi: 10.1139/bcb-2022-0027
[13]	Wang J, Ge S, Wang Y, et al. Puerarin alleviates UUO-induced inflammation and fibrosis by regulating the NF-κB P65/STAT3 and TGFβ1/smads signaling pathways[J]. Drug Des Dev Ther, 2021, 15: 3697-3708. doi: 10.2147/DDDT.S321879
[14]	贾迎起, 张敏, 李彪. 放射性核素标记的成纤维细胞活化蛋白抑制剂正电子发射断层扫描在心脏疾病诊断中的研究进展[J]. 诊断学理论与实践, 2025, 24(2): 220-225. doi: 10.16150/j.1671-2870.2025.02.014
[15]	Chen G, Xu H, Xu T, et al. Calycosin reduces myocardial fibrosis and improves cardiac function in post-myocardial infarction mice by suppressing TGFBR1 signaling pathways[J]. Phytomedicine, 2022, 104: 154277. doi: 10.1016/j.phymed.2022.154277
[16]	Qin W, Cao L, Massey I Y. Role of PI3K/Akt signaling pathway in cardiac fibrosis[J]. Mol Cell Biochem, 2021, 476(11): 4045-4059. doi: 10.1007/s11010-021-04219-w
[17]	Yang W, Wu Z, Yang K, et al. BMI1 promotes cardiac fibrosis in ischemia-induced heart failure via the PTEN-PI3K/Akt-mTOR signaling pathway[J]. Am J Physiol Heart Circ Physiol, 2019, 316(1): H61-H69. doi: 10.1152/ajpheart.00487.2018
[18]	Stempien-Otero A, Kim D H, Davis J. Molecular networks underlying myofibroblast fate and fibrosis[J]. J Mol Cell Cardiol, 2016, 97: 153-161. doi: 10.1016/j.yjmcc.2016.05.002
[19]	Tang Q, Markby G R, MacNair A J, et al. TGF-β-induced PI3K/AKT/mTOR pathway controls myofibroblast differentiation and secretory phenotype of valvular interstitial cells through the modulation of cellular senescence in a naturally occurring in vitro canine model of myxomatous mitral valve disease[J]. Cell Prolif, 2023, 56(6): e13435. doi: 10.1111/cpr.13435

Relative Articles(20)

Relative Articles

[1]	Xiaoxia SHEN, Chunhui FENG, Xiaodong ZHAO. Effects of Stem Cells on Myocardial Infarction Repair and Cardiac Electrophysiology Based on Exosomal STAT3 Protein Transport. Journal of Kunming Medical University, doi: 10.12259/j.issn.2095-610X.S20251207
[2]	Changyong WU, Rui WANG, Suli BAO, Ruijie LI, Huang SUN, Yujia YE, Fei XU, Yunzhu PENG. Effects of Exercise Rehabilitation on Cardiac Fibrosis and Function in Rats with Myocardial Infarction. Journal of Kunming Medical University, doi: 10.12259/j.issn.2095-610X.S20231004
[3]	Cong LIU, Guishuai WU, Rui PU, Shude LI, Jianping TAO, Renfa ZHANG. EGCG Improves Myocardial Fibrosis Induced by High Fat and High Sugar Diet in Obese Rats by Inhibiting TGF-β1/Smads Signaling Pathway. Journal of Kunming Medical University, doi: 10.12259/j.issn.2095-610X.S20220506
[4]	Wang Jun, Zhang Yi , Zhang Shi Hui , Jin Fu Yu , Li Tian , Xu Hong . . Journal of Kunming Medical University,
[5]	Cao Yu Ting , Wang Qi Xian , Yang Ping . . Journal of Kunming Medical University,
[6]	Zhang Ru Qiang , Ma Yuan Ping , Lv Pin Die , Liu Ping , Wang Fang . Risk Factors of Myocardial Infarction in Chinese Han Population of Yunnan Province. Journal of Kunming Medical University,
[7]	Wu Jian . Construction of Ischemic Cardiomyopathy Model via Ligation of Left Anterior Descending Artery by using Diannan Miniporcine. Journal of Kunming Medical University,
[8]	Li Qiang . Clinical Study on Autologous Peripheral Blood Stem Cells Transplantation for Myocardial infarction. Journal of Kunming Medical University,
[9]	Chen Jian . . Journal of Kunming Medical University,
[10]	ShaikhRezwanhussian. . Journal of Kunming Medical University,
[11]	Liu Li Li . . Journal of Kunming Medical University,
[12]	Li Fu Ping . . Journal of Kunming Medical University,
[13]	Chen Li Hua . 碎裂QRS波与心肌梗死研究现状和进展. Journal of Kunming Medical University,
[14]	Bai Xiang Feng . . Journal of Kunming Medical University,
[15]	Zhang Ping . . Journal of Kunming Medical University,
[16]	Chen Xiao Guang . . Journal of Kunming Medical University,
[17]	Chen Xiao Guang . . Journal of Kunming Medical University,
[18]	Huang Ning Yu . . Journal of Kunming Medical University,
[19]	Sun Hai Mei . 缺血后处理对猪非梗死区心肌细胞凋亡的影响. Journal of Kunming Medical University,
[20]	. . Journal of Kunming Medical University,