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作 者:马静[1] 赵坤霄[1] 赵林林[1] 解汝娟[1]
机构地区:[1]哈尔滨医科大学附属第一医院肾内科,黑龙江哈尔滨150001
出 处:《哈尔滨医科大学学报》2013年第5期397-400,共4页Journal of Harbin Medical University
基 金:黑龙江省教育厅2010年度科学技术研究项目(11551191)
摘 要:目的研究匹格列酮对各种应激条件下肾小球系膜细胞的保护作用,进一步探讨匹格列酮保护糖尿病肾病的作用机制。方法分别以高葡萄糖、糖基化终产物和过氧化氢孵育大鼠肾小球系膜细胞(mesangial cells,MCs);以p38促分裂原活化蛋白激酶(p38MAPK)信号通路特异性抑制剂SB203580和匹格列酮(pioglitazone,PO)分别预处理RMCs,再给予上述3种刺激因素孵育RMCs,观察RMCs中磷酸化p38MAPK、核因子(NF-κB)和转化生长因子(TGF-β)蛋白表达。结果与各刺激组相比,匹格列酮预处理的肾小球系膜细胞p38MAPK、NF-κB和TGF-β蛋白表达水平降低。结论匹格列酮对肾小球系膜细胞具有一定的保护作用,保护机制可能与其抑制p38MAPK信号通路激活及减少NF-κB、TGF-β的表达相关。Objective To study the protective effect of pioglitazone on glomerular mesangial cells(MCs) cultured under many stimulant conditions and to investigate its possible mecha- nism. Methods MCs were incubated with high glucose(HG) , advanced glycation end prod- uct (AGE), H202 and MCs were pretreated with the inhibitor of p38MAPK(SB203580) and pioglitazone (PO) , then were incubated with above stimulant factors. Expression of proteins of P38MAPK, NF-KB and TGF-β in MCs were observed. Results Pioglitazone obviously de- creased expression of p-p38MAPK, TGF-β and NF-KB. Conclusion MCs to a degree and the mechanism has a relation to the inhibition of way, TGF-β and NF-KB. Pioglitazone can protect p38MAPK signal path-
关 键 词:p38促分裂原活化蛋白激酶 NF—KB TGF—β 匹格列酮 肾小球系膜细胞
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