Effects of Oleanolic Acid on Myocardial Injury in Diabetic Mice by Regulating Phosphatidylinositol 3 Kinase/Protein Kinase B/Glucose Transporter Type 4 Signalling Pathway

内科学 内分泌学 乳酸脱氢酶 丙二醛 磷脂酰肌醇 葡萄糖转运蛋白 肌酸激酶 超氧化物歧化酶 医学 氧化应激 激酶 化学 生物化学 胰岛素
作者
Zengqing Sun,Xinyu Shang,Jiashuo Li,Jinkun Xi,Xing Fengmei,Wan Liang,Xin Yu,Sheng Han,Shuang Zhao
出处
期刊:Indian Journal of Pharmaceutical Sciences [Medknow]
卷期号:85 (1)
标识
DOI:10.36468/pharmaceutical-sciences.1087
摘要

One of the leading causes of diabetes-related deaths is myocardial damage, which may be the cause of heart failure in people with type 2 diabetes mellitus. The objective of the research was to look at the impact of coronary failure with kind a pair of type 2 diabetes mellitus. This project aimed to explore the protective impact of oleanolic acid on myocardial damage in type 2 diabetes mellitus and to investigate the connected mechanism. Specific pathogen free grade db/db male mice were elected as model, while the Db/m mice were opted for control. Different doses of drug intervention were performed and the general condition, cardiac function, blood glucose, blood lipids, degree of myocardial injury, and degree of oxidative stress were examined by morphological examination of myocardial tissues, biochemical examination, and gene and protein amount detection. The results showed that lactate dehydrogenase, creatine kinase isoenzyme, total cholesterol, triglycerides and malondialdehyde levels in serum of Db/db mice were increased, while phosphatidylinositol 3 kinase, protein kinase B, glucose transporter 4 expression and superoxide dismutase level in myocardial tissue were decreased. After using oleanolic acid, the serum concentrations of lactate dehydrogenase, creatine kinase isoenzyme, total cholesterol, triglycerides and malondialdehyde were declined in Db/db mice, while phosphatidylinositol 3 kinase, protein kinase B, glucose transporter 4 expression and superoxide dismutase level were rised. The results recommend that oleanolic acid has protective impact on cardiac muscle injury in Db/db mice and conjointly the mechanism could also be correlated with promoting the activation of phosphatidylinositol 3 kinase/protein kinase B/glucose transporter 4 signal transduction.
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