Protective Effect of Epigallocatechin Gallate on Diabetic Rat Hearts via TGF-β1/Smad3 Signaling Pathway
10.12007/j.issn.0258-4646.2019.02.006
- VernacularTitle:表没食子儿茶素没食子酸酯对糖尿病大鼠心脏的保护作用及对TGF-β1/Smad3信号通路表达的影响
- Author:
Jingru SUN
1
;
Keyan CHEN
;
Qian SUN
;
Mei HAN
Author Information
1. 辽宁省金秋医院内分泌科
- Keywords:
epigallocatechin gallate;
diabetic cardiomyopathy;
signal pathway
- From:
Journal of China Medical University
2019;48(2):119-123
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of Epigallocatechin gallate (EGCG) on cardiac protection in diabetic rats and the expression of TGF-1/Smad3 signaling pathway. Methods The influence of clean level 40 SD rats, weight 200-220 g, divided into four random groups:control (Sham) group, diabetic cardiomyopathy model (DC) group, EGCG group, and metformin positive control group (Met).Post 8 weeks of high-fat-diet administration, the rats were injected intraperitoneally with STZ to establish the diabetes cardiomyopathy model. Upon successful model establishment, the EGCG group was intraperitoneally injected with EGCG and the cardiac function of the rats was measured after 28 days of drug administration. Then, the pathological results of the myocardial tissue were analyzed. Triglyceride (TG), total cholesterol (TC), glycosylated hemoglobin (HbA1 c), and blood glucose (FBG) concentrations were also measured. Further, the concentrations of superoxide dismutases (SOD), malondialdehyde (MDA), catalase (CAT), and glutathione peroxidase (GPX) in serum were measured by ELISA. The expression of TGF-β1 and Smad3 in kidney tissues of the rats was measured by Western blotting analysis. Results EGCG could reduce the glucose, lipid, and MDA levels in the blood of the diabetic rats, enhance cardiac systolic and diastolic functions, inhibit TGF-β1 and Smad3 protein expression, enhance the activity of SOD, CAT and GPX, and reduce myocardial tissue fibrosis. Conclusion EGCG can protect diabetic rat hearts by improving metabolic disorder, and its mechanism may be related to the oxidative-stress mediated by the TGF-β1/Smad3 signaling pathway.
