| 周月宏,田坚,沈静雪,等.过表达SOCS2对人肾小球系膜细胞中炎性因子表达的影响及其机制研究[J].安徽医药,2016,20(2):295-299. |
| 过表达SOCS2对人肾小球系膜细胞中炎性因子表达的影响及其机制研究 |
| Effect and mechanism of overexpressing SOCS2 on the expression of inflammatory cytokines in human glomerular mesangial cells |
| 投稿时间：2015-09-18 |
| DOI： |
| 中文关键词: SOCS2 糖尿病肾病 JAK/STAT 肾小球系膜细胞 |
| 英文关键词: SOCS2 diabetic nephropathy JAK/STAT glomerular mesangial cells |
| 基金项目:沈阳市科技计划项目基金(No F13-220-9-10) |
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| 中文摘要: |
| 目的 建立过表达SOCS2的HMCs细胞模型,检测各组HMCs中JAK/STAT信号通路的活性,观察DN炎性因子的表达,明确过表达SOCS2对细胞模型的影响及作用机制。方法 通过腺病毒感染的方法使细胞模型中过表达SOCS2,实验分为CG组、CG+Ad-null组、CG+Ad-SOCS2组、HG组、HG+Ad-null组、HG+Ad-SOCS2组。Western blot方法检测各组细胞模型中JAK/STAT信号通路的活化情况。ELISA方法检测各组细胞培养上清中IL-6、TNF-α的表达。结果 与CG组相比,高糖诱导后的HG组、HG+Ad-null组、HG+Ad-SOCS2组中p-JAK2、P-STAT3、IL-6、TNF-α的表达量均升高(P<0.01)；与HG组相比,HG+Ad-SOCS2组中这些指标均显著下降(P<0.01),而HG+Ad-null组则无显著差异。结论 SOCS2通过抑制JAK/STAT信号通路来降低细胞模型中炎性因子IL-6、TNF-α的表达。 |
| 英文摘要: |
| Objective Established the HMCs cell model of SOCS2 overexpressing cells,detected the activation of JAK/STAT signaling pathway in HMCs,observed the expression of inflammatory cytokines of DN in cells,and clarified mechanisms of the effect of SOCS2 in cell model.Methods The overexpression of SOCS2 in the cell model was realized by the method of adenovirus infection,and cells were divided into CG group,CG+Ad-null group,CG+Ad-SOCS2 group,HG group,HG+Ad-null group,and HG+Ad-SOCS2 group.The activation of JAK/STAT signaling pathway in the cell model of each group was detected by western blot.The expressions of IL-6 and TNF-αin culture supernatant of each group were detected by ELISA.Results Compared with CG group,the expressions of p-JAK2,P-STAT3,IL-6 and TNF-α were significantly increased in HG group,HG+Ad-null group and HG+Ad-SOCS2 group (P<0.01).And the expressions of these factors in HG+Ad-SOCS2 group were significantly decreased compared with HG group(P<0.01),and those of HG+Ad-null group had no significant difference. Conclusions SOCS2 can reduce the expressions of inflammatory cytokines IL-6 and TNF-α by inhibiting JAK/STAT in cell model. |
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