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姜黄素的抗糖尿病作用主要与其在肝脏中的抗细胞凋亡作用和 PI3K/Akt 信号通路调节有关。

Curcumin anti-diabetic effect mainly correlates with its anti-apoptotic actions and PI3K/Akt signal pathway regulation in the liver.

机构信息

College of Life Sciences, Nankai University, Tianjin, 300071, China.

College of Life Sciences, Nankai University, Tianjin, 300071, China.

出版信息

Food Chem Toxicol. 2020 Dec;146:111803. doi: 10.1016/j.fct.2020.111803. Epub 2020 Oct 6.

DOI:10.1016/j.fct.2020.111803
PMID:33035629
Abstract

This study aimed to investigate the therapeutic effect of curcumin on type 2 diabetes and its underlying mechanisms. A type 2 diabetes mellitus rat model was established by providing high-fat diet and low doses of streptozotocin. Type 2 diabetes mellitus rats were treated with low dose and high dose of curcumin for 8 weeks. The results showed that high-dose curcumin significantly reduced fasting blood glucose, total cholesterol, triglyceride, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, alanine aminotransferase, and aspartate transaminase, liver coefficient, and malondialdehyde levels, and BCL2-Associated X expression in the type 2 diabetes mellitus rats. High-dose curcumin increased the levels of liver superoxide dismutase, catalase, and glutathione; as well as the expression of liver B-cell lymphoma-2, phosphatidylinositol 3-kinase, phosphorylated phosphatidylinositol 3-kinase, protein kinase B, and phosphorylated protein kinase B in type 2 diabetes mellitus rats. Furthermore, it ameliorated the histological structure of the liver and pancreas in diabetes mellitus model rats. However, low-dose curcumin had no significant effect on diabetes mellitus model rats. The results suggest that adequate doses of curcumin controls type 2 diabetes mellitus development as well as the mechanism involved in its anti-apoptotic actions and phosphatidylinositol 3-hydroxy kinase/protein kinase B signal pathway regulation in the liver.

摘要

本研究旨在探讨姜黄素对 2 型糖尿病的治疗作用及其作用机制。通过给予高脂肪饮食和低剂量链脲佐菌素建立 2 型糖尿病大鼠模型。用低剂量和高剂量姜黄素治疗 2 型糖尿病大鼠 8 周。结果表明,高剂量姜黄素可显著降低 2 型糖尿病大鼠的空腹血糖、总胆固醇、甘油三酯、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、丙氨酸氨基转移酶、天冬氨酸氨基转移酶、肝系数和丙二醛水平,以及 BCL2 相关 X 的表达。高剂量姜黄素增加了肝超氧化物歧化酶、过氧化氢酶和谷胱甘肽的水平;以及肝 B 细胞淋巴瘤-2、磷酸肌醇 3-激酶、磷酸化磷酸肌醇 3-激酶、蛋白激酶 B 和磷酸化蛋白激酶 B 在 2 型糖尿病大鼠中的表达。此外,它改善了糖尿病模型大鼠的肝和胰腺组织学结构。然而,低剂量姜黄素对糖尿病模型大鼠没有显著影响。结果表明,足够剂量的姜黄素可控制 2 型糖尿病的发展,以及其在肝脏中的抗细胞凋亡作用及其对磷酸肌醇 3-激酶/蛋白激酶 B 信号通路的调节机制。

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