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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。
Objective To investigate the effect of rosiglitazone on the TGF-β1 / Smad signal transduction pathway in lung tissue of spontaneously type 2 diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats. Methods Sixteen OLETF rats were divided into untreated OLETF group and eight OLETF / L treated groups (OLETF / L group). Eight Long Evans Tokushima Otsuka (LETO) rats were used as control group. The expression of TGF-β1, Smad2, Smad3, Smad7, fibronectin (FN) and type Ⅲ collagen in lung tissue of each group were analyzed by immunohistochemistry. Results Compared with LETO group, the expression of TGF-β1, Smad2, Smad3, FN and type Ⅲ collagen in OLETF group was significantly increased (P <0.01) and the expression of Smad7 was significantly decreased in OLETF group (P < The expression of TGF-β1, Smad2, Smad3, FN and collagen type Ⅲ in L group was significantly lower than that in OLETF group (P <0.01), while Smad7 expression was significantly increased (P <0.01). Conclusion Rosiglitazone may prevent diabetic pulmonary fibrosis by regulating the TGF-β1 / Smad signaling pathway.