黄芪甲苷Ⅳ对内毒素诱导RAW264.7细胞损伤的保护作用及机制研究  

Protective Effect and Molecular Mechanism of Astragaloside IV on LPS-induced Macrophage RAW264.7 Injury

作　　者：覃华[1] 张琰[1] 杜小燕[1] 韩艳[1] 王茹[1] 

机构地区：[1]第四军医大学唐都医院药剂科,陕西西安710038

出　　处：《现代生物医学进展》2013年第11期2040-2043,共4页Progress in Modern Biomedicine

摘　　要：目的:研究黄芪皂苷IV对LPS诱导的巨噬细胞RAW264.7损伤的保护作用及机制。方法:测定细胞活力判断心肌细胞损伤的程度。TNF-α,IL-1β,IL-6,IL-10的释放以及NF-κB蛋白、Akt和磷酸化Akt表达用以研究作用机制。结果:黄芪皂苷IV对LPS引起的RAW264.7细胞损伤具有显著的抑制作用,1,3和10μM黄芪皂苷IV可显著降低LPS诱导的RAW264.7细胞TNF-α,IL-1β和IL-6的生成,促进IL-10的释放。黄芪皂苷IV剂量依赖性地增加了由LPS刺激而引起的RAW264.7细胞NF-κB蛋白的表达,抑制了LPS所致的p-Akt蛋白表达的升高。结论:黄芪皂苷IV可通过Akt-NF-κB途径调控促炎因子和抗炎因子表达的失衡,有效发挥对LPS诱导巨噬细胞RAW264.7损伤的保护作用。Objective： To investigate the protective effect and molecular mechanisms of Astragaloside IV on LPS-induced macrophage RAW264.7 injury. Methods： Anti-inflammatory responses and signal transduction including TNF-of, IL-113, IL-6 and IL-10 generation as well as the activation of Akt, p-Akt, and NF-κB were detected. Results： 1, 3 and 10 μM Astragaloside IV protected LPS-induced macrophage RAW264.7 from injury, significantly decreased TNF-et, IL-1 [3 and 1L-6 production and significantly increased IL-10 release in a concentration-dependent manner. Astragaloside IV suppressed the expression of NF-κB protein and the activation of p-Akt induced by LPS. Conclusions： Astmgaloside IV blocks NF-κB activation by interfering with Akt phosphorylation to suppress LPS-induced injury in RAW264.7 macrophages.

关 键 词：黄芪皂苷IV 脂多糖 巨噬细胞 细胞因子 细胞核因子-ΚB 

分 类 号：R282.71[医药卫生—中药学]