红景天苷通过调节p38和JNK信号通路抑制BV-2细胞分泌炎性因子
王杰^*, 张艳玲, 庄楠
潍坊护理职业学院，潍坊 262500
摘要
红景天苷是传统中药红景天的主要成分，已有研究显示红景天苷具有一定的抗炎性作用。本研究旨在探讨红景天苷对BV-2细胞炎性反应的调节作用及可能机制。实验分为对照组、脂多糖(lipopolysaccharide, LPS)组、红景天苷组、红景天苷预处理+LPS组，用100 μg/L LPS和/或10 mg/L红景天苷处理BV-2细胞，收集细胞培养基上清(条件培养基)，采用real-time PCR方法检测细胞IL-6和 TNF-α mRNA表达水平，ELSIA方法检测培养基IL-6和TNF-α含量，条件培养基处理PC12细胞24 h后，Hoechst 33258染色检测细胞核形态学改变，cell counting kit 8 (CCK-8)试剂盒检测细胞活力，免疫印迹方法检测BV-2细胞p38和JNK的磷酸化水平。结果表明100 μg/L LPS处理可显著提高BV-2细胞内IL-6和TNF-α的表达水平(P < 0.05)。红景天苷可显著下调LPS诱导的BV-2细胞IL-6和TNF-α表达量(P < 0.05)，下调p38和JNK的磷酸化水平(P < 0.05)。SB202190和SP600125可降低LPS引起的IL-6和TNF-α表达，与红景天苷共处理后可拮抗LPS的诱导效应。与LPS组相比，红景天苷预处理+ LPS组的条件培养基处理后，PC12细胞的细胞活力显著升高(P < 0.05)，同时细胞核固缩和聚集情况减少(P < 0.05)。以上结果提示，红景天苷可在一定程度上抑制小胶质细胞活动，通过调节p38和JNK信号通路减少炎性因子释放，从而降低PC12细胞的损伤。
关键词： 红景天苷; 炎性反应; 细胞凋亡; PC12
分类号：Q189

Salidroside inhibits inflammatory factor release in BV-2 cells through p38 and JNK pathways
WANG Jie^*, ZHANG Yan-Ling, ZHUANG Nan
Weifang Nursing Vocational College, Weifang 262500, China
Abstract
Salidroside is the major bioactive component of Rhodiolasachalinensis. Studies have shown that salidroside has anti-
inflammatory effects. In the present study, we ex&shy;amined whether salidroside inhibited inflammatory reaction in BV-2 microglial cells and thereby inhibited PC12 apoptosis. BV-2 cells were induced by lipopolysaccharides (LPS, 100 μg/L) and/or salidroside (10 mg/L), and then the conditioned medium was collected. Real time-PCR was used to detect IL-6 and TNF-α mRNA expression. The contents of IL-6 and TNF-α in medium were detected by ELSIA. Conditioned medium was added to PC12 culture medium and cell counting kit-8 and Hoechst 33258 were used to assess cell viability and cell apoptosis, respectively, after 24 h of incubation. The levels of phospho-p38 mitogen-activated protein kinase (p-p38) and phospho-c-Jun N-terminal kinase (p-JNK) in BV-2 cells were examined by Western blot analysis. The result showed that salidroside pretreatment decreased the expression of IL-6 and TNF-α as well as phosphorylation of p38 and JNK induced by LPS in BV-2 cells. The inhibitors of p38 (SB202190) and JNK (SP600125) could reduce IL-6 and TNF-α mRNA expression that was induced by LPS. Combined utilization of SB202190, SP600125 and salidroside could attenuate the effects of LPS. After conditioned medium treatment, PC12 cell viability and cell apoptosis were ameliorated in salidroside pretreatment + LPS group compared with LPS group. These results suggest that salidroside inhibits PC12 cell apoptosis by decreasing inflammatory factor release as well as p38 and JNK activation in activated microglia.
Key words: salidroside; inflammation; apoptosis; PC12

收稿日期：2017-05-02　　录用日期：2017-10-10
通讯作者：王杰　　E-mail: 15853603713@163.com
DOI: 10.13294/j.aps.2018.0017
引用本文：
王杰, 张艳玲, 庄楠. 红景天苷通过调节p38和JNK信号通路抑制BV-2细胞分泌炎性因子[J]. 生理学报 2018; 70 (3): 245-252.
WANG Jie, ZHANG Yan-Ling, ZHUANG Nan. Salidroside inhibits inflammatory factor release in BV-2 cells through p38 and JNK pathways. Acta Physiol Sin 2018; 70 (3): 245-252 (in Chinese with English abstract).



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