Dendrobium Nobile Polysaccharide Improves Myocardial Injury in Diabetic Rats by Regulating Plin5 Mediated Fatty Acid β Oxidation of Cardiomyocytes

Jizhou LI; Hongwei LI; Shengyu TANG; Zejun JIANG; Mengmeng GUO; Yatian LI; Hongling YANG

doi:10.12259/j.issn.2095-610X.S20241002

Volume 45 Issue 10

Oct. 2024

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Jizhou LI, Hongwei LI, Shengyu TANG, Zejun JIANG, Mengmeng GUO, Yatian LI, Hongling YANG. Dendrobium Nobile Polysaccharide Improves Myocardial Injury in Diabetic Rats by Regulating Plin5 Mediated Fatty Acid β Oxidation of Cardiomyocytes[J]. Journal of Kunming Medical University, 2024, 45(10): 8-16. doi: 10.12259/j.issn.2095-610X.S20241002

Citation:

Jizhou LI, Hongwei LI, Shengyu TANG, Zejun JIANG, Mengmeng GUO, Yatian LI, Hongling YANG. Dendrobium Nobile Polysaccharide Improves Myocardial Injury in Diabetic Rats by Regulating Plin5 Mediated Fatty Acid β Oxidation of Cardiomyocytes[J]. Journal of Kunming Medical University, 2024, 45(10): 8-16. doi: 10.12259/j.issn.2095-610X.S20241002

Citation:

Jizhou LI, Hongwei LI, Shengyu TANG, Zejun JIANG, Mengmeng GUO, Yatian LI, Hongling YANG. Dendrobium Nobile Polysaccharide Improves Myocardial Injury in Diabetic Rats by Regulating Plin5 Mediated Fatty Acid β Oxidation of Cardiomyocytes[J]. Journal of Kunming Medical University, 2024, 45(10): 8-16. doi: 10.12259/j.issn.2095-610X.S20241002

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Dendrobium Nobile Polysaccharide Improves Myocardial Injury in Diabetic Rats by Regulating Plin5 Mediated Fatty Acid β Oxidation of Cardiomyocytes

doi: 10.12259/j.issn.2095-610X.S20241002

1.
School of Clinical Medicine University，Dali University，Dali Yunnan 671003
2.
Dept. of Cardiovascular Medicine，The 3rd People’s Hospital of Yunnan Province，Kunming Yunnan 650011，China

Received Date: 2024-07-10
Available Online: 2024-10-19
Publish Date: 2024-10-31

Abstract

Abstract

Objective To explore the mechanism of Dendrobium nobium polysaccharide on myocardial injury in diabetic rats by regulating the fatty acid β oxidation signaling pathway of cardiomyocytes from Plin5. Methods A total of 72 male SD rats of a clean grade were divided into a control group （n = 10） and a modeling group （n = 62）. The control group was fed regular diet, while the modeling group was given a high-fat, high-sugar diet for two months, along with a single STZ injection to establish a diabetic myocardial injury animal model. After successfully creating the model, the modeling group of SD rats was further divided into five subgroups: the model group, the isosorbide mononitrate tablet group, the low-dose Dendrobium nobium polysaccharide group, the medium-dose group, and the high-dose group （n = 10）. After 4 weeks of drug treatment, rats were euthanized, and their hearts were collected to detect the myocardial hemopathology （using HE and Masson staining）, lipid levels （TG, TC, HDL-C and LDL-C）, inflammatory factors （IL-1α, IL-1β, IL-6 and TNF-α） and antioxidant indexes （SOD, GSH, MDA and ROS）. Blood samples were taken to assess cardiac function, insulin and blood sugar levels, and Western blot was used to detect the expression characteristics of Plin5, SCD1, CPT1A, ACOX1 and PPARα proteins. Results Histopathology with HE and Masson staining showed that in the normal group, the myocardial fibers of rats were neatly arranged, whereas in the model group, there was fibrous rupture. Compared to the model group, different degrees of improvement were seen in all treatment groups with Dendrobium polysaccharides. Blood sugar and insulin resistance index increased in the model group compared to the normal group （P < 0.05）, with insulin levels decreasing （P < 0.05）. Compared to the model group, the three groups treated with Dendrobium polysaccharides showed reduced blood sugar and insulin resistance index （P < 0.05）. In the low-dose, mid-dose, and isosorbide dinitrate tablet groups, insulin levels did not increase （P > 0.05）, while the high-dose Dendrobium polysaccharides group exhibited an increase in insulin content （P < 0.05）. Compared to the normal group, TG, TC and LDL-C in the model group were remarkably increased （P < 0.05）, while HDL-C was remarkably decreased （P < 0.05）. Compared to the model group, TG, TC and LDL-C in the three Dendrobium polysaccharide groups and the positive drug group were remarkably decreased （P < 0.05）, while HDL-C was remarkably increased （P < 0.05）. Compared to the normal group, AST, CK, CK-MB, LDH, a-HBDH and CTnl in the model group were remarkably increased （P < 0.05）. Compared to the model group, the above 6 indexes in the 3 Dendrobium polysaccharide treatment groups and positive drug group were remarkably decreased （P < 0.05）. Compared to the normal group, IL-1α, IL-1β, IL-6 and TNF-α in the the model group were remarkably increased （P < 0.05）, and they were remarkably decreased in the three Dendrobium polysaccharide treatment groups and the positive drug group compared to the model group （P < 0.05）; compared to normal group, SOD and GSH in model group were remarkably decreased （P < 0.05）, MDA and ROS were remarkably increased （P < 0.05）, compared to the model group, SOD and GSH in the three treatment groups and the positive drug group were increased （P < 0.05）, while MDA and ROS were decreased （P < 0.05）. Compared to normal group, Plin5 and SCD1 in model group were increased （P < 0.05）, and protein expressions of PPARα, CPT1 and ACOX1 were decreased （P < 0.05）. Compared to model group, Plin5 and SCD1 were remarkably increased （P < 0.05）. Compared to the model group, Plin5 and SCD1 were remarkably decreased in all treatment groups and positive drug groups （P < 0.05）, while PPARα, CPT1 and ACOX1 were remarkably increased （P < 0.05）. Conclusion Dendrobium nobium polysaccharide can regulate fatty acid β oxidation through Plin5, thereby reducing myocardial lipid content, inflammation, and oxidative stress, protecting diabetic myocardial injury in rats, and improving heart function.
- Dendrobium nobile polysaccharide,
- Plin5,
- Fattyacid βoxidation,
- Diabetic myocardial injury

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