脂多糖通过JAK2/STAT3通路诱导肾小球内皮细胞炎症反应的研究  

The JAK2/STAT3 signaling pathway is involved in the inflammation induced by lipopolysaccharide in glomerular endothelial cells

作　　者：刘燕[1] 张晓翠[1] 邓芳[1] Liu Yan;Zhang Xiaocui;Deng Fang(Dept of Pediatrics,The First Affiliated Hospital of Anhui Medical University,Hefei 230022)

机构地区：[1]安徽医科大学第一附属医院儿科,合肥230022

出　　处：《安徽医科大学学报》2020年第3期327-332,共6页Acta Universitatis Medicinalis Anhui

基　　金：安徽省公益性技术应用研究联动计划项目(编号:1704f0804027);安徽省教育厅高校优秀拔尖人才培育项目(编号:gxbjZD07)。

摘　　要：目的研究脂多糖(LPS)对小鼠肾小球内皮细胞(mGECs)炎症反应的影响及机制。方法对mGECs进行分离培养,使用CCK-8及Western blot确定LPS的最佳刺激浓度。体外LPS刺激mGECs后,利用JAK2-siRNA、STAT3-siRNA进行干预,用ELISA及qRT-PCR方法检测mGECs的肿瘤坏死因子(TNF-α)、白细胞介素6(IL-6)的表达及分泌水平;用Western blot检测JAK2和STAT3蛋白表达及磷酸化水平。结果与对照组相比,LPS刺激后mGECs表达JAK2和STAT3磷酸化水平呈浓度依赖性升高(P<0.05),细胞培养上清液中TNF-α、IL-6分泌增多(P<0.05),且JAK2 siRNA、STAT3 siRNA能有效抑制LPS诱导的TNF-α、IL-6过表达(P<0.05)。结论 JAK2/STAT3信号通路参与了LPS诱导的mGECs炎症的发生。Objective To investigate the potential mechanism of lipopolysaccharide(LPS)′s effect on inflammatory response of mouse glomerular endothelial cells(mGECs).Methods Isolation and culture of mGECs, CCK-8 assay and Western blot were used to determine the optimum concentration of LPS. mGECs were stimulated with LPS and incubated with JAK2 siRNA, STAT3 siRNA in vitro. The mRNA expression and secretion levels of tumor necrosis factor(TNF-α) and interleukin-6(IL-6) were detected by ELISA and qRT-PCR. JAK2 and STAT3 protein expressions and the phosphorylation level were detected respectively by Western blot.Results Compared with the control group, the expressions of JAK2 and STAT3 phosphorylation in mGECs increased in a concentration-dependent manner after LPS stimulation(P<0.05). The secretion of TNF-α, IL-6 in cell culture medium markedly increased(P<0.05). JAK2 siRNA and STAT3 siRNA could significantly inhibit the overexpression of TNF-α and IL-6 induced by LPS(P<0.05).Conclusion The JAK2/STAT3 signaling pathway is involved in the development of LPS-induced mGECs inflammation.

关 键 词：肾小球内皮细胞 JAK2 STAT3 炎症 脂多糖 

分 类 号：R363[医药卫生—病理学] R692[医药卫生—基础医学]