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丹酚酸B通过AMPK途径改善db/db小鼠的高血糖和血脂异常。

Salvianolic Acid B Ameliorates Hyperglycemia and Dyslipidemia in db/db Mice through the AMPK Pathway.

作者信息

Huang Ming-Qing, Zhou Cai-Jie, Zhang Yi-Ping, Zhang Xiao-Qin, Xu Wen, Lin Jing, Wang Pei-Jian

机构信息

College of Pharmacy, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China.

出版信息

Cell Physiol Biochem. 2016;40(5):933-943. doi: 10.1159/000453151. Epub 2016 Dec 7.

Abstract

BACKGROUND/AIMS: Salvianolic acid B (Sal B), a major polyphenolic compound of Salvia miltiorrhiza Bunge, has been shown to possess potential antidiabetic activities. However, the action mechanism of SalB in type 2 diabetes has not been investigated extensively. The present study was designed to investigate the effects of Sal B on diabetes-related metabolic changes in a spontaneous model of type 2 diabetes, as well as its potential molecular mechanism.

METHODS

Male C57BL/KsJ-db/db mice were orally treated with Sal B (50 and 100 mg/kg) or metformin (positive drug, 300 mg/kg) for 6 weeks.

RESULTS

Both doses of Sal B significantly decreased fasting blood glucose, serum insulin, triglyceride and free fatty acid levels, reduced hepatic gluconeogenic gene expression and improved insulin intolerance in db/db mice. High dose Sal B also significantly improved glucose intolerance, increased hepatic glycolytic gene expression and muscle glycogen content, and ameliorated histopathological alterations of pancreas, similar to metformin. Sal B treatment resulted in increased phosphorylated AMP-activated protein kinase (p-AMPK) protein expression in skeletal muscle and liver, increased glucose transporter 4 (GLUT4) and glycogen synthase protein expressions in skeletal muscle, and increased peroxisome proliferator-activated receptor alpha (PPARα) and phosphorylated acetyl CoA carboxylase (p-ACC) protein expressions in liver.

CONCLUSION

Our data suggest that Sal B displays beneficial effects in the prevention and treatment of type 2 diabetes at least in part via modulation of the AMPK pathway.

摘要

背景/目的:丹酚酸B(Sal B)是丹参的一种主要多酚类化合物,已显示具有潜在的抗糖尿病活性。然而,Sal B在2型糖尿病中的作用机制尚未得到广泛研究。本研究旨在探讨Sal B对2型糖尿病自发模型中糖尿病相关代谢变化的影响及其潜在的分子机制。

方法

雄性C57BL/KsJ-db/db小鼠口服给予Sal B(50和100 mg/kg)或二甲双胍(阳性药物,300 mg/kg),持续6周。

结果

两种剂量的Sal B均显著降低了db/db小鼠的空腹血糖、血清胰岛素、甘油三酯和游离脂肪酸水平,降低了肝脏糖异生基因表达,改善了胰岛素抵抗。高剂量Sal B还显著改善了葡萄糖耐量,增加了肝脏糖酵解基因表达和肌肉糖原含量,并改善了胰腺的组织病理学改变,与二甲双胍相似。Sal B治疗导致骨骼肌和肝脏中磷酸化的AMP激活蛋白激酶(p-AMPK)蛋白表达增加,骨骼肌中葡萄糖转运蛋白4(GLUT4)和糖原合酶蛋白表达增加,肝脏中过氧化物酶体增殖物激活受体α(PPARα)和磷酸化乙酰辅酶A羧化酶(p-ACC)蛋白表达增加。

结论

我们的数据表明,Sal B至少部分通过调节AMPK途径对2型糖尿病的预防和治疗具有有益作用。

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