p^(38)MAPK在IL-18诱导肾小管上皮细胞转分化中的作用  

Interleukin-18-induced transdifferentiation in renal proximal tubular cells is mediated by activation of p38MAPK pathway

作　　者：张军峰[1] 姚翠微[1] 刘华锋[1] 梁东[1] 陈孝文[1] 

机构地区：[1]广东医学院附属医院肾病研究所,湛江524001

出　　处：《中国应用生理学杂志》2010年第2期199-201,共3页Chinese Journal of Applied Physiology

基　　金：广东省自然科学基金资助(5011589)

摘　　要：目的:白细胞介素18(IL-18)可诱导肾小管上皮细胞转分化,本研究探讨其是否是通过p38MAPK途径而起作用。方法:应用不同浓度的p38MAPK通路特异性阻断剂SB203580(0、5、10、20μmol/L)预孵育人近端肾小管上皮细胞(HK-2细胞)30min后,加入IL-18(100ng/ml)共培养24、48、72h。应用RT-PCR法检测α-平滑肌肌动蛋白(α-SMA)mRNA的表达水平;应用ELISA法测定细胞浆中α-SMA蛋白质含量。结果:SB203580呈剂量依赖性地抑制IL-18诱导的HK-2细胞α-SMA基因表达(P<0.05)。结论:p38MAPK通路是调控IL-18诱导肾小管上皮细胞转分化的主要信号通路之一。Objective：To explore the effect of p38MAPK signaling pathway in interleukin-18-induced transdifferentiation in renal proximal tubular cells.Methods：Human proximal tubular epithelial cell line （HK-2 cells） was cultured in vitro.After preincubated with SB203580（0,5,10,20 μmol/L） for 30 minutes,cells were exposed to IL-18（100 ng/ml） for 24,48 and 72 hours respectively.The expressions of α-smooth actin（α-SMA） in cultured HK-2 cells were assessed by RT-PCR and ELISA.Results：IL-18-induced expressions of α-SMA mRNA and protein were inhibited obviously by a dose-dependent manner when HK-2 cells were incubated with SB203580（0,5,10,20 μmol/L） and IL-18（100 ng/ml） for different time（P0.05）.Conclusion：IL-18-induced transdifferentiation of renal tubular epithelial cells（RTECs） is suppressed obviously by blocking p38MAPK signaling pathways.IL-18-induced transdifferentiation of RTECs is probably mediated,at least in part,through the activation of p38MAPK signaling pathways.

关 键 词：肾间质纤维化 肾小管上皮细胞 转分化 白细胞介素-18 P38MAPK 

分 类 号：R692.6[医药卫生—泌尿科学]