【摘要】 目的探讨罗格列酮对自发性2型糖尿病Otsuka Long-Evans Tokushima Fatty(OLETF)大鼠肺组织转化生长因子(TGF)-β1/Smad信号转导途径的影响。方法 OLETF大鼠16只,分为未治疗的OLETF组和接受罗格列酮治疗组(OLETF/L组)各8只,设Long Evans Tokushima Otsuka(LETO)大鼠8只为对照组。免疫组织化学分析各组大鼠肺组织TGF-β1、Smad2、Smad3、Smad7、纤维连接蛋白(FN)和Ⅲ型胶原表达。结果与LETO组大鼠相比,OLETF组大鼠肺组织TGF-β1、Smad2、Smad3、FN和Ⅲ型胶原表达均显著增加(P<0.01),Smad7表达显著减少(P<0.01);OLETF/L组比OLETF组大鼠肺组织TGF-β1、Smad2、Smad3、FN和Ⅲ型胶原表达均显著减少(P<0.01),Smad7表达显著增加(P<0.01)。结论罗格列酮可能通过调控TGF-β1/Smad信号转导途径抗糖尿病肺纤维化。更多还原

【Abstract】 Objective To approach the effects of rosiglitazone treatment on transforming growth factor-β1/Smad(TGF-β1/Smad) signaling pathways in Otsuka Long-Evans Tokushima Fatty(OLETF) rats.Methods Experimental rats were divided into three groups: OLETF group,rosiglitazone-treated group(OLETF/L group) and Long Evans Tokushima Otsuka rats(LETO group) as control,8 rats in each group.The expression of TGF-β1,Smad2,Smad3,Smad7,fibronectin(FN),and collagen type Ⅲ in rat lungs were examined by immunohistochemistry.Results The expressions of TGF-β1,Smad2,Smad3,FN and collagen type Ⅲ increased in OLETF rat lungs than those of LETO rats(P < 0.01),while the expression of Smad7 decreased in OLETF group(P < 0.01).The expressions of TGF-β1,Smad2,Smad3,FN and collagen type Ⅲ decreased in OLETF/L group than those of the OLETF group(P < 0.01),and the expression of Smad7 increased in OLETF/L group(P < 0.01).Conclusion Rosiglitazone may improve diabetic pulmonary fibrosis probably by regulating TGF-β1/ Smad signaling pathways.更多还原