期刊
BMC COMPLEMENTARY MEDICINE AND THERAPIES
卷 23, 期 1, 页码 -出版社
BMC
DOI: 10.1186/s12906-022-03818-4
关键词
Oxymatrine; Diabetes; Oxidative stress; Apoptosis; Myocardial injury; Inflammation
This study evaluated the protective effects of oxymatrine (OMT) in myocardial injury caused by type 2 diabetes mellitus. Diabetic rats were treated with OMT orally for 8 weeks, and the results showed that OMT alleviated myocardial injury by reducing blood glucose and oxidative stress and promoting the expression of antioxidative enzymes and the Nrf2/HO-1 pathway.
The necessity of increasing the efficiency of organ preservation has encouraged researchers to explore the mechanisms underlying diabetes-related myocardial injuries. This study intended to evaluate the protective effects of oxymatrine (OMT) in myocardial injury caused by type 2 diabetes mellitus. A model of diabetic rats was established to simulate type 2 diabetes mellitus using an intraperitoneal injection of a single dose of 65 mg/kg streptozotocin with a high-fat and high-cholesterol diet, and diabetic rats were subsequently treated with OMT (60, 120 mg/kg) by gavage for 8 weeks. Thereafter, diabetic rats demonstrated notable decreases in left ventricular systolic pressure (LVSP), +/- dp/dt(max), and in the activities of glutathione peroxidase, superoxide dismutase, and catalase. Moreover, we found notable increases in left ventricular end-diastolic pressure, fasting blood glucose, and malondialdehyde, as well as changes in cell apoptosis and decreased expression levels of Nrf2, HO-1, tyrosine protein kinase JAK (JAK), and signal transducer and transcription activator (STAT). Treatment with OMT alleviated all of the measured parameters. Collectively, these findings suggest that activation of the Nrf2/HO-1 and inhibition of the JAK/STAT signaling are involved in mediating the cardioprotective effects of OMT and also highlight the benefits of OMT in ameliorating myocardial injury in diabetic rats.
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