原花青素抑制脂多糖激活神经小胶质细胞的机制

doi:10.3969/j.issn.1004-616x.2018.02.004

癌变·畸变·突变 ›› 2018, Vol. 30 ›› Issue (2): 98-102.doi: 10.3969/j.issn.1004-616x.2018.02.004

原花青素抑制脂多糖激活神经小胶质细胞的机制

张妍^1,2, 张小强^1,2, 梁晓瑜^1,2, 王旭^1,2, 刘静^1,2

1. 东南大学公共卫生学院, 江苏南京 210009;
2. 东南大学环境医学工程教育部重点实验室, 江苏南京 210009

收稿日期:2017-11-23 修回日期:2018-03-02 出版日期:2018-03-30 发布日期:2018-03-30
通讯作者: 张小强,E-mail:zhangxq7843@126.com E-mail:zhangxq7843@126.com
作者简介:张妍,E-mail:zyzyljs@126.com
基金资助:
中央高校基本科研业务费专项资金资助和江苏省普通高校研究生科研创新计划资助项目（SJZZ16_0034）

Mechanism of proanthocyanidin-mediated inhibition of LPS-induced activation of microglial cells

ZHANG Yan^1,2, ZHANG Xiaoqiang^1,2, LIANG Xiaoyu^1,2, WANG Xu^1,2, LIU Jing^1,2

1. School of Public Health, Southeast University, Nanjing 210009;
2. Key Laboratory of Environmental Medicine, Engineering of Ministry of Education, Southeast University, Nanjing 210009, Jiangsu, China

Received:2017-11-23 Revised:2018-03-02 Online:2018-03-30 Published:2018-03-30

摘要/Abstract

摘要： 目的：研究原花青素抑制脂多糖（LPS）激活神经小胶质细胞的机制。方法：采用1.0 μg/mL LPS刺激神经小胶质细胞建立体外炎症模型，再用不同浓度（0.1、0.5、2.5、10.0 μg/mL）原花青素进行干预，四甲基噻唑蓝（MTT）法检测不同浓度原花青素对神经小胶质细胞的毒性，ELISA法检测炎症因子TNF-α、IL-1β、IL-6的表达，Western blot法检测TLR4、p38、p-p38蛋白的表达。结果：与对照组比较，1.0 μg/mL LPS组TNF-α、IL-1β、IL-6水平均显著升高（P < 0.05），TLR4和p-p38蛋白表达亦显著增加（P < 0.05）；给予不同浓度原花青素干预后，与1.0 μg/mL LPS组比较，炎性因子TNF-α、IL-1β、IL-6分泌水平均下降（P均 < 0.05），TLR4和p-p38蛋白表达水平均显著下调（P均 < 0.05）。结论：原花青素可能通过TLR4/p38 MAPK信号通路抑制脂多糖激活神经小胶质细胞。

关键词: 原花青素, 脂多糖, 小胶质细胞, TLR4, p38 MAPK

Abstract: OBJECTIVE: The present study was designed to investigate the possible mechanisms of proanthocyanidin-mediated inhibition in lipopolysaccharide (LPS)-induced activation of microglial BV2 cells. METHODS: An inflammation cell model was produced in BV2 cells which were treated with LPS (1.0 μg/mL). In addition,cells were treated with proanthocyanidins (0.1,0.5,2.5,10.0 μg/mL) prior to LPS exposure and MTT assay was used to detect the viability of BV2 cells. The level of inflammatory cytokines TNF-α,IL-1β and IL-6 were examined by ELISA method. TLR4 and p38,p-p38 MAPK protein expressions were examined by the Western blot analysis. RESULTS: Compared with the control group,LPS (1.0 μg/mL) significantly increased the expression of TLR4 and p-p38 protein as well as the release of inflammatory mediator TNF-α,IL-1β and IL-6 (P < 0.05). Proanthocyanidin significantly inhibited LPS-induced production of inflammatory mediators in a dose-dependent manner (P < 0.05). Moreover,PC significantly inhibited the phosphorylation of p38 and TLR4 expression (P < 0.05). CONCLUSION: Proanthocyanidin inhibited inflammatory mediator expression by suppressing TLR4 mediated p38 MAPK signaling pathways in LPS-stimulated BV2 cells.

Key words: proanthocyanidin, lipopolysaccharide, microglia, TLR4, p38 MAPK

中图分类号:

R994.6

张妍, 张小强, 梁晓瑜, 王旭, 刘静. 原花青素抑制脂多糖激活神经小胶质细胞的机制[J]. 癌变·畸变·突变, 2018, 30(2): 98-102.

ZHANG Yan, ZHANG Xiaoqiang, LIANG Xiaoyu, WANG Xu, LIU Jing. Mechanism of proanthocyanidin-mediated inhibition of LPS-induced activation of microglial cells[J]. Carcinogenesis, Teratogenesis & Mutagenesis, 2018, 30(2): 98-102.

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原花青素抑制脂多糖激活神经小胶质细胞的机制

Mechanism of proanthocyanidin-mediated inhibition of LPS-induced activation of microglial cells

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