LXRs过表达抑制高糖诱导的H9C2细胞炎症反应及其机制  

Over-expression of LXRs inhibiting the inflammatory response of H9C2 cells induced by high glucose and its mechanism

作　　者：周江龙 王云开[2] 欧阳先国 黄瑛 ZHOU Jiang-Long;WANG Yun-Kai;OUYANG Xian-Guo(The Third Hospital of Nanchang City,Nanchang 330009,Jiangxi,China)

机构地区：[1]南昌市第三医院,江西南昌330009 [2]南昌大学第一附属医院

出　　处：《中国老年学杂志》2020年第22期4831-4834,共4页Chinese Journal of Gerontology

基　　金：国家自然科学基金项目(No.81160117)。

摘　　要：目的探讨慢病毒介导的肝X受体(LXRs)过表达对高糖诱导的H9C2细胞炎症反应的作用及其作用机制。方法体外培养H9C2细胞,利用高糖诱导建立心肌细胞炎症反应,构建过表达LXRs慢病毒载体,并将其转染H9C2细胞中。72 h后CCK-8检测细胞增殖抑制率;qRT-PCR分别检测LXRs和炎症因子人单核细胞趋化蛋白(MCP)-1、白细胞介素(IL)-6、人肿瘤坏死因子(TNF)-αmRNA表达;Western印迹检测核因子(NF)-κB蛋白表达水平及细胞免疫荧光观察其核转位。结果过表达LXRs可改善高糖引起的细胞增殖抑制,并显著下调高糖诱导的MCP-1、IL-6、TNF-αmRNA及NF-κB蛋白表达(P<0.01)。结论过表达LXRs可抑制高糖诱导的心肌细胞炎症反应,其机制与抑制NF-κB信号通路有关。Objective To observe the effect of LXRs over-expression mediated by lentivirus on the inflammatory response of H9C2 cells induced by high glucose and explore its mechanism.Methods H9C2 cells were cultured in vitro.Inflammatory reaction of cardiomyocytes was established by high glucose,the lentivirus vector with over-expression of LXRs was constructed and transfected into H9C2 cells.After 72 hours of lentivirus infection,CCK-8 was used to detect the proliferation inhibition rate of H9C2 cells.Meanwhile,the expressions of LXRs,MCP-1,IL-6,TNF-αmRNA were detected by qRT-PCR,Western blot and immunofluorescence were used to detect the expression of NF-κB phosphorylation protein.Results Over-expression of LXRs could improve the inhibition of cell proliferation induced by high glucose and significantly down-regulate the expressions of MCP-1,IL-6,TNF-αand NF-κB induced by high glucose(P<0.01).Conclusions Over-expression of LXRs could inhibit high glucose-induced inflammatory responses in cardiomyocytes via the NF-κB signaling pathway.

关 键 词：LXRs 高糖 炎症 核因子(NF)-κB信号通路 

分 类 号：R542.2[医药卫生—心血管疾病]