Lipopolysaccharide-induced activation of microglia through JAK2-STAT3 pathway

郝玉通; 陈纯海; 杨学森; 余争平

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Lipopolysaccharide-induced activation of microglia through JAK2-STAT3 pathway

更新时间：2026-01-09

- Lipopolysaccharide-induced activation of microglia through JAK2-STAT3 pathway
- Journal of Army Medical University Vol. 31, Issue 12, Pages: 1119-1122(2009)
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  CLC： R322.81;R329.25;R392.3
- Published：2009
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郝玉通,陈纯海,杨学森,余争平.JAK2/STAT3信号通路参与脂多糖诱导小胶质细胞活化的研究[J].陆军军医大学学报(原第三军医大学学报),2009,31(12):1119-1122.

　HAO Yu-tong,CHEN Chun-hai,YANG Xue-sen,YU Zheng-ping.Lipopolysaccharide-induced activation of microglia through JAK2-STAT3 pathway[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(12):1119-1122.
郝玉通,陈纯海,杨学森,余争平.JAK2/STAT3信号通路参与脂多糖诱导小胶质细胞活化的研究[J].陆军军医大学学报(原第三军医大学学报),2009,31(12):1119-1122. DOI：

　HAO Yu-tong,CHEN Chun-hai,YANG Xue-sen,YU Zheng-ping.Lipopolysaccharide-induced activation of microglia through JAK2-STAT3 pathway[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(12):1119-1122. DOI：

摘要

目的研究蛋白酪氨酸激酶2/信号转导子与激活子3(Janus kinase signal transducers 2 and activator of transcription 3，JAK2/STAT3)信号通路参与脂多糖(LPS)诱导小胶质细胞(MG)活化的影响及其可能机制。方法用细胞免疫组织化学的方法观察小胶质细胞特异性标志物OX-42的变化，用ELISA方法检测LPS刺激后肿瘤坏死因子（TNF-α）的表达变化。以及用Western blot方法检测JAK2和STAT3磷酸化变化水平。结果 LPS刺激后OX-42阳性细胞数显著增强，分泌大量的细胞因子TNF-α，JAK2和STAT3磷酸化水平显著升高，并被抑制剂AG490有效抑制。结论 JAK2-STAT3信号通路参与了LPS诱导的小胶质细胞活化。JAK2-STAT3通路激活与炎症因子分泌有关。

Abstract

Objective To investigate the effects of JAK2-STAT3 signaling pathway on lipopolysaccharide(LPS)-induced activation of microglia and the possible mechanisms. Methods Immunohistochemistry and flow cytometry were applied to observe the changes in OX-42. Changes in TNF-α expression after stimulation with LPS were detected by ELISA. The phosphorylation levels of JAK2 and STAT3 were detected by Western-blot. Results LPS stimulation significantly increased the number of the positive cells of OX-42

enhanced TNF-α expression

and up-regulated the phosphorylation level of JAK2 and STAT3. Conclusion LPS may induce the microglia activation through the activation of the JAK2-STAT3 signaling pathway and promote the secretion of TNF-α

suggesting that activation of the JAK2-STAT3 signaling pathway may be associated with the secretion of the inflammatory factors.

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