哈尔滨医科大学学报
哈爾濱醫科大學學報
합이빈의과대학학보
JOURNAL OF HARBIN MEDICAL UNIVERSITY
2013年
5期
397-400
,共4页
马静%赵坤霄%赵林林%解汝娟
馬靜%趙坤霄%趙林林%解汝娟
마정%조곤소%조림림%해여연
p38促分裂原活化蛋白激酶%NF-κB%TGF-β%匹格列酮%肾小球系膜细胞
p38促分裂原活化蛋白激酶%NF-κB%TGF-β%匹格列酮%腎小毬繫膜細胞
p38촉분렬원활화단백격매%NF-κB%TGF-β%필격렬동%신소구계막세포
p38 MAPK%NF-κB%TGF-β%pioglitazone%mesangial cell
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。
目的：研究匹格列酮對各種應激條件下腎小毬繫膜細胞的保護作用，進一步探討匹格列酮保護糖尿病腎病的作用機製。方法分彆以高葡萄糖、糖基化終產物和過氧化氫孵育大鼠腎小毬繫膜細胞（mesangial cells， MCs ）；以p38促分裂原活化蛋白激酶（p38MAPK）信號通路特異性抑製劑 SB203580和匹格列酮（pioglitazone， PO ）分彆預處理RMCs，再給予上述3種刺激因素孵育RMCs，觀察RMCs 中燐痠化p38MAPK、覈因子（NF-κB）和轉化生長因子（TGF-β）蛋白錶達。結果與各刺激組相比，匹格列酮預處理的腎小毬繫膜細胞p38MAPK、NF-κB和TGF-β蛋白錶達水平降低。結論匹格列酮對腎小毬繫膜細胞具有一定的保護作用，保護機製可能與其抑製p38MAPK信號通路激活及減少 NF-κB 、TGF-β的錶達相關。
목적：연구필격렬동대각충응격조건하신소구계막세포적보호작용，진일보탐토필격렬동보호당뇨병신병적작용궤제。방법분별이고포도당、당기화종산물화과양화경부육대서신소구계막세포（mesangial cells， MCs ）；이p38촉분렬원활화단백격매（p38MAPK）신호통로특이성억제제 SB203580화필격렬동（pioglitazone， PO ）분별예처리RMCs，재급여상술3충자격인소부육RMCs，관찰RMCs 중린산화p38MAPK、핵인자（NF-κB）화전화생장인자（TGF-β）단백표체。결과여각자격조상비，필격렬동예처리적신소구계막세포p38MAPK、NF-κB화TGF-β단백표체수평강저。결론필격렬동대신소구계막세포구유일정적보호작용，보호궤제가능여기억제p38MAPK신호통로격활급감소 NF-κB 、TGF-β적표체상관。
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), H2O2 and MCs were pretreated with the inhibitor of p38MAPK(SB203580) and pioglitazone ( PO) , then were incubated with above stimulant factors .Expression of proteins of P38 MAPK, NF-κB and TGF-βin MCs were observed .Results Pioglitazone obviously de-creased expression of p-p38MAPK, TGF-βand NF-κB.Conclusion Pioglitazone can protect MCs to a degree and the mechanism has a relation to the inhibition of p 38 MAPK signal path-way, TGF-βand NF-κB.
