丙泊酚对小胶质细胞炎症因子的影响及其机制研究

丙泊酚对小胶质细胞炎症因子的影响及其机制研究
叶雪飞;左春龙;梅虹霞;苏颖;杨建平
【期刊名称】《中国现代医学杂志》
【年(卷),期】2018(028)002
【摘要】Objective To investigate the effect of Propofol on inflammatory cytokines in microglia and its mechanism. Methods Microglial BV-2 cells were divided into control group, Propofol group, lipopolysaccharide (LPS) group, and LPS+Propofol group. The cells of the control group were added with PBS. The cells of the Propofol group were added with 30 μmol/L Propofol. The cells of the LPS group were treated with 1 μg/ml LPS. The
ce lls of the LPS+Propofol group were added with 30 μmol/L Propofol and 1 μg/ml LPS. The cell viability was determined by MTT colorimetric assay. The levels of interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in supernatant wer e measured by ELISA. The expressions of p38MAPK and TLR4 mRNAs were detected by RT-PCR. The expressions of p38MAPK and TLR4 proteins were detected by Western blot. Results The activity of microglia in the LPS group and the LPS+Propofol group were lower than that in the control group and the Propofol group (P < 0.05). The activity of microglia in the LPS+Propofol group was higher than that in the LPS group (P < 0.05). The levels of IL-1β, IL-6 and TNF-α in the supernatant of the LPS group and the LPS+Propofol group were higher than those in the control group and the Propofol group (P < 0.05). The
levels of IL-1β, IL-6 and TNF-α in the supernatant of the LPS+Propofol group were lower than those in the LPS group (P < 0.05). The mRNA and protein expressions of p38MAPK and TLR4 in the LPS group and the
LPS+Propofol group were higher than those in the control group and the Propofol group (P < 0.05). The mRNA and protein expressions of
p38MAPK and TLR4 in the LPS+Propofol group were lower than those in the LPS group (P < 0.05). There were no significant differences in the above indices between the Propofol group and the control group (P > 0.05). Conclusions Propofol has the effect of inhibiting the hyperactivity and inflammatory response of microglia, and its mechanism may be related to the down-regulation of TLR4-p38MAPK signaling pathway.%目的探讨丙泊酚对小胶质细胞炎症因子的影响及其机制.方法将小胶质BV-2细胞分为对照组、丙泊酚组、脂多糖(LPS)组、LPS+丙泊酚组,对照组细胞加入PBS液,丙泊酚组细胞加入丙泊酚30μmol/L,LPS组细胞加入LPS 1μg/ml,LPS+丙泊酚组细胞加入丙泊酚30μmol/L+LPS 1μg/ml.采用MTT比色实验测定细胞活性,采用酶联免疫吸附法测定细胞上清液中白细胞介素1β(IL-1β)、白细胞介素6(IL-6)、肿瘤坏死因子-α(TNF-α)水平,采用逆转录-聚合酶链反应测定细胞p38MAPK和TLR4 mRNA的表达,采用Western blot检测细胞p38MAPK和TLR4蛋白表达量.结果LPS组和LPS+丙泊酚组小胶质细胞活性低于对照组和丙泊酚组(P<0.05),LPS+丙泊酚组小胶质细胞活性高于LPS组(P<0.05);LPS组和LPS+丙泊酚组小胶质细胞上清液中IL-1β、IL-6、TNF-α 水平高于对照组和丙泊酚组(P<0.05),LPS+丙泊酚组小胶质细胞上清液中IL-1β、IL-6、TNF-α 水平低于LPS组(P<0.05);LPS组和LPS+丙泊酚组小胶质细胞p38MAPK、TLR4 mRNA和蛋白表达量高于对照组和丙泊酚组(P<0.05),LPS+丙泊酚组小胶质细胞p38MAPK、TLR4 mRNA和蛋白表
达量低于LPS组(P<0.05);丙泊酚组和对照组小胶质细胞各指标比较,差异无统计学意义(P>0.05).结论丙泊酚能抑制小胶质细胞过度活化和炎症反应,其机制可能与丙泊酚可下调TLR4-p38MAPK信号通路有关.
【总页数】4页(P33-36)
【作者】叶雪飞;左春龙;梅虹霞;苏颖;杨建平
【作者单位】苏州大学附属第一医院麻醉科,江苏苏州 215006;温州医科大学附属第二医院麻醉科,浙江温州 325000;温州医科大学附属第二医院麻醉科,浙江温州325000;温州医科大学附属第二医院麻醉科,浙江温州 325000;苏州大学附属第一医院麻醉科,江苏苏州 215006
【正文语种】中文
【中图分类】R614
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