Inhibitory effect of ginsenoside Rg1 on lipopolysaccharide-induced microglial activation in mice
Inhibitory effect of ginsenoside Rg1 on lipopolysaccharide-induced microglial activation in mice
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人参皂苷Rg1对脂多糖诱导的小鼠小胶质细胞活化的抑制作用
DOI：
10.1016/j.brainres.2010.11.069
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发表时间：
2011-02-16
期刊：
影响因子：
2.9
通讯作者：
Chen, Nai-Hong
中科院分区：
文献类型：
--
作者：
Hu, Jin-Feng;Song, Xiu-Yun;Chen, Nai-Hong
小胶质细胞激活通过产生各种促炎细胞因子和一氧化氮（NO）在神经退行性疾病的发病机制中起关键作用。本文研究了人参皂苷Rg1对脑室注射脂多糖（LPS）小鼠的抗炎作用。口服Rg1后，大鼠大脑皮质和海马组织中NO和肿瘤坏死因子(TNF)- α的产生均呈剂量依赖性降低。lps注射组大鼠大脑皮层和海马组织中离子钙结合适配器分子1 （Iba-1）的表达均高于对照组。然而，Rg1通过抑制Iba-1的表达来抑制小胶质细胞的激活。Rg1抑制了诱导型一氧化氮合酶（iNOS）的表达。Rg1抑制I κ B磷酸化水平、NF κ B p65亚基核易位以及LPS诱导的p38、ERK1/2、JNK丝裂原活化蛋白激酶（MAPK）磷酸化水平。综上所述，Rg1通过抑制NF κ B和MAPK通路抑制LPS介导的炎症，从而解释了其对神经退行性疾病的治疗作用。(C) 2010 Elsevier B.V.版权所有
Microglial activation plays a pivotal role in the pathogenesis of neurodegenerative diseases by producing various pro-inflammatory cytokines and nitric oxide (NO). In the paper, the anti-inflammatory effect of ginsenoside Rg1 was investigated in mice intracerebroventricular injected of lipopolysaccharide (LPS). NO and tumor necrosis factor (TNF)-alpha production in both cerebral cortex and hippocampus decreased at dose-dependent manner by oral administration with Rg1. And the expression of ionized calcium binding adaptor molecule 1 (Iba-1) increased in both cerebral cortex and hippocampus in LPS-injected group compared to that in control group. However, Rg1 inhibited microglial activation by suppressing Iba-1 expression. In addition, the expression of inducible nitric oxide synthase (iNOS) was inhibited by Rg1. Moreover, Rg1 suppressed the phosphorylation level of I kappa B, nuclear translocation of p65 subunit of NF kappa B, and phosphorylation level of p38, ERK1/2, JNK mitogen-activated protein kinase (MAPK) induced by LPS. Concluding, Rg1 inhibited the inflammation mediated by LPS by suppressing NF kappa B and MAPK pathway, which provided the explanation for its therapeutic effect on neurodegenerative diseases. (C) 2010 Elsevier B.V. All rights reserved.