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恩格列净抑制 SGLT2 可减轻糖尿病小鼠心脏的心肌氧化应激和纤维化。

SGLT2 inhibition with empagliflozin attenuates myocardial oxidative stress and fibrosis in diabetic mice heart.

机构信息

NHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin, 300070, China.

出版信息

Cardiovasc Diabetol. 2019 Feb 2;18(1):15. doi: 10.1186/s12933-019-0816-2.

DOI:10.1186/s12933-019-0816-2
PMID:30710997
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6359811/
Abstract

BACKGROUND

Hyperglycaemia associated with myocardial oxidative stress and fibrosis is the main cause of diabetic cardiomyopathy. Empagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor has recently been reported to improve glycaemic control in patients with type 2 diabetes in an insulin-independent manner. The aim of this study was to investigate the effect of empagliflozin on myocardium injury and the potential mechanism in type 2 diabetic KK-Ay mice.

METHODS

Thirty diabetic KK-Ay mice were administered empagliflozin (10 mg/kg/day) by oral gavage daily for 8 weeks. After 8 weeks, heart structure and function were evaluated by echocardiography. Oxidants and antioxidants were measured and cardiac fibrosis was analysed using immunohistochemistry, Masson's trichrome stain and Western blot.

RESULTS

Results showed that empagliflozin improved diabetic myocardial structure and function, decreased myocardial oxidative stress and ameliorated myocardial fibrosis. Further study indicated that empagliflozin suppressed oxidative stress and fibrosis through inhibition of the transforming growth factor β/Smad pathway and activation of Nrf2/ARE signaling.

CONCLUSIONS

Glycaemic control with empagliflozin significantly ameliorated myocardial oxidative stress injury and cardiac fibrosis in diabetic mice. Taken together, these results indicate that the empagliflozin is a promising agent for the prevention and treatment of diabetic cardiomyopathy.

摘要

背景

与心肌氧化应激和纤维化相关的高血糖是糖尿病心肌病的主要原因。钠-葡萄糖共转运蛋白 2（SGLT2）抑制剂恩格列净最近被报道以胰岛素非依赖的方式改善 2 型糖尿病患者的血糖控制。本研究旨在探讨恩格列净对 2 型糖尿病 KK-Ay 小鼠心肌损伤的影响及其潜在机制。

方法

30 只糖尿病 KK-Ay 小鼠每天经口灌胃给予恩格列净（10mg/kg/天），持续 8 周。8 周后，通过超声心动图评估心脏结构和功能。采用免疫组化、Masson 三色染色和 Western blot 分析氧化剂和抗氧化剂，分析心肌纤维化。

结果

结果表明，恩格列净改善了糖尿病心肌结构和功能，降低了心肌氧化应激，改善了心肌纤维化。进一步的研究表明，恩格列净通过抑制转化生长因子 β/Smad 通路和激活 Nrf2/ARE 信号通路抑制氧化应激和纤维化。

结论

恩格列净的血糖控制显著改善了糖尿病小鼠的心肌氧化应激损伤和心脏纤维化。综上所述，这些结果表明恩格列净是预防和治疗糖尿病心肌病的有前途的药物。

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