摘要
目的:探讨核因子-κB(NF-κB)/IκB信号通路在血管紧张素Ⅱ(Ang Ⅱ)诱导的肾小球系膜细胞促炎性细胞因子表达中的作用。方法:应用核酸酶保护法检测系膜细胞肿瘤坏死因子α(TNF-α)、IL-1α和IL-1β mRNA表达;应用凝胶电泳迁移率和Western blot检测肾小球系膜细胞中NF-κB活化、p65亚基核转让以及IκBα和IκBβ的降解。结果:正常培养状态下,系膜细胞可组成型表达TNF-α和IL-1β,而不表达IL-1αmRNA,AngⅡ刺激后促炎性细胞因子表达显著上调,NF-κB特异性抑制剂2-疏代氨基甲酸吡咯烷显著抑制Ang Ⅱ诱导的促炎性细胞因子基因表达;Ang Ⅱ诱导系膜细胞NF-κB活化,p65核转位及胞质内IκBα和IκBα的降解。结论:Ang Ⅱ诱导肾小球系膜细胞中促炎性细胞因子表达可能通过NF-κB/IκB信号转导通路来实现。
Objective:To investigate the role of NF-KB/lKB signal pathway in the regulation of proinflammatory cytokines in Ang II-induced human mesangial cells (HMC) . Methods: TNF-a, IL-la and IL-lp mRNA expression was determined by ribonuclease protection assay. Electrophoretic mobility shift assay (EMSA) and Western Blot were used to detect the activity of NF-kB and degradation of 1KB. Results: HMC incubated in medium alone did not express IL-la mRNA, but there was constitutive mRNA expression TNFa and IL-1b in unstimulated cells. Ang II significantly upregulated TNF-a, IL-1a and IL-1b mRNA expression. Significant up-regulation of NF-KB activation, nuclear translocation of p65 subunit, and degradation of IkBa and IkBb were observed in Ang II-induced HMC. Conclusions: Expression of proinflammatory cytokines in Ang Il-induce HMC was mediated by NF-KB/lKB signal pathway.
出处
《南京医科大学学报（自然科学版）》
CAS
CSCD
北大核心
2003年第6期530-532,共3页
Journal of Nanjing Medical University(Natural Sciences)
基金
国家自然科学基金(30100081)
江苏省教委自然科学基金(02KJD320011)
