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作 者:闫慧明[1] 刘河红 张雪[1] 张丽霞[1] 闫师 薛一萍 孙英梅 YAN Hui-ming;LIU He-hong;ZHANG Xue;ZHANG Li-xia;YAN Shi;XUE Yi-ping;SUN Ying-mei
机构地区:[1]内蒙古科技大学包头医学院第二附属医院,内蒙古包头014030
出 处:《风湿病与关节炎》2024年第6期1-4,10,共5页Rheumatism and Arthritis
基 金:2022年度内蒙古自治区高等学校科学技术研究项目(NJZY22083)。
摘 要:目的:观察miR-146a调控TLRs信号通路对活动期类风湿关节炎患者外周血单个核细胞的影响。方法:选取20例活动期类风湿关节炎患者,对患者外周血单个核细胞分离培养,分为LPS组和LPS+miR-146a组;同时选取10例健康体检者为健康对照组。采用MTT法测定吸光度,比较外周血单个核细胞变化,检测外周血单个核细胞的凋亡情况。RT-PCR法检测外周血单个核细胞miR-146a、Toll样受体2(TLR2)、髓样分化因子88(MyD88)mRNA表达。Western blot法检测外周血单个核细胞miR-146a、TLR2、MyD88蛋白表达。结果:LPS组较健康对照组和LPS+miR-146a组外周血单个核细胞TLR2表达明显升高(P<0.05);LPS组较健康对照组和LPS+miR-146a组外周血单个核细胞中miR-146a、TLR2、MyD88 mRNA表达明显升高(P<0.05);LPS组较健康对照组和LPS+miR-146a组外周血单个核细胞miR-146a、TLR2、MyD88蛋白表达明显升高(P<0.05)。结论:高表达miR-146a可能通过依赖TLR2/MyD88信号通路,抑制活动期类风湿关节炎患者外周血单个核细胞中TLR2、MyD88表达,减轻炎症反应。Objective:To observe the effect of miR-46 regulation of TLRs signaling pathway on peripheral blood mononuclear cells in patients with active rheumatoid arthritis.Methods:Twenty patients with active rheumatoid arthritis were selected and divided into the LPS group and the LPS+miR-146a group,and peripheral blood mononuclear cells in them were isolated and cultured.At the same time,ten healthy examinees were selected as the healthy control group.MTT method was used to measure absorbance,changes in peripheral blood mononuclear cells were compared,and apoptosis of peripheral blood mononuclear cells was detected.RT-PCR was used to detect the mRNA expression of miR-146a,TLR2,and MyD88 in peripheral blood mononuclear cells.Protein immunoblotting was used to detect the protein expression of miR-146a,TLR2,and MyD88 in peripheral blood mononuclear cells.Results:The TLR2 expression rate of peripheral blood mononuclear cells in the LPS group was significantly increased compared to the healthy control group and the LPS+miR-146a group(P<0.05);the expression of protein mRNA of miR-146a,TLR2,and MyD88 in peripheral blood mononuclear cells of the LPS group was significantly increased compared to the healthy control group and the LPS+miR-146a group(P<0.05);the protein levels of miR-146a,TLR2,and MyD88 in peripheral blood mononuclear cells were significantly increased in the LPS group compared to the healthy control group and the LPS+miR-146a group(P<0.05).Conclusion:High expression may inhibit the expression of TLR2 and MyD88 in peripheral blood mononuclear cells of patients with active rheumatoid arthritis by relying on the TLR2/MyD88 signaling pathway,reducing inflammatory response.
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