限热联合灵桂助肝汤可改善棕榈酸诱导的胰岛素抵抗

Li Zhang , Ting-ying Zhang , Zi-heng Ye, Jia-hao Feng, Jin Zhao, Peng Huang, Jian Qin, Jia-pan Sun, Tao-li Liu
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引用次数: 0

摘要

目的探讨热量限制(CR)联合灵桂柱肝制剂血清对胰岛素抵抗(IR)的影响及其可能机制。方法采用灵归助肝汤(LGZGD)或等量生理盐水灌胃1周作为空白对照,取腹主动脉血制备灵归助肝汤药物血清或对照血清。将HepG2细胞与正常对照培养基或30% CR培养基中添加LGZGD药物血清或对照血清孵育24 h,然后暴露于250 μM棕榈酸(PA)中24 h,检测细胞葡萄糖摄取的变化以评估胰岛素抵抗的改善,并通过western blotting和qPCR检测AKT、p-AKT和AS160的表达变化。结果单纯限热(30%)和LGZGD药物血清治疗均能显著改善PA诱导的细胞糖摄取减少和AKT/p-AKT/AS160信号下调,且联合干预组效果显著大于单一干预组。探讨灵归蠲饮可增强CR对HepG2细胞胰岛素抵抗的改善作用。其潜在机制可能与调节AKT/p-AKT/AS160信号通路有关,需要通过敲除实验和体内研究进一步验证。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Caloric restriction combined with Linggui Zhugan Decoction improves palmitic acid-induced insulin resistance

Caloric restriction combined with Linggui Zhugan Decoction improves palmitic acid-induced insulin resistance

Introduction

To explore the effects and probable mechanisms of caloric restriction (CR) combined with Linggui Zhugan pharmaceutic serum on insulin resistance (IR).

Methods

Sprague–Dawley rats were treated with Linggui Zhugan decoction (LGZGD) or equivalent amount of saline as blank control by gavage for one week, after which blood was collected from the abdominal aorta to prepare LGZGD pharmaceutic serum or control serum. HepG2 cells were incubated with normal control medium or 30 % CR culture medium supplemented with LGZGD pharmaceutic serum or control serum for 24 h and then exposed to 250 μM palmitic acid (PA) for another 24 h. Changes in cellular glucose uptake were detected to evaluate the improvements in insulin resistance, and changes in the expression changes of AKT, p-AKT, and AS160 were detected via western blotting and qPCR.

Results

Both simple caloric restriction (30 %) and LGZGD pharmaceutic serum treatment significantly improved the decrease in cellular glucose uptake and the downregulation of AKT/p-AKT/AS160 signaling induced by PA, and the combined intervention group had a significantly greater effect than the single intervention groups.

Discussion

Linggui Zhugan decoction can enhance the effects of CR on improving insulin resistance in HepG2 cells. The potential mechanism may be related to the modulation of AKT/p-AKT/AS160 signaling, which needs to be verified further with knock-down experiment and in vivo study.
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