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目的探讨罗格列酮对自发性糖尿病OLETF(Otsuka Long-Evans Tokushima Fatty)大鼠肺组织纤维化的影响及其机制。方法 30周龄雄性OLETF大鼠16只,随机分为糖尿病组(DM组)和罗格列酮组(RGT组,予罗格列酮3mg·kg-1·d-1灌胃12周),对照组为LETO(Long Evans Tokushima Otsuka)大鼠8只。HE、Masson染色观察各组大鼠肺组织结构及其胶原沉积变化,免疫印迹(Westernblotting)方法检测肺组织Smad3、Smad7和Ⅲ型胶原表达,ELISA检测肺组织转化生长因子β(1transforming growth factor-β1,TGF-β1)的表达。结果与对照组大鼠相比,DM组大鼠肺组织TGF-β1、Smad3和Ⅲ型胶原表达增加,Smad7表达减少,差异均有统计学意义(P<0.05),肺组织胶原沉积增加,呈纤维化趋势;罗格列酮治疗可使RGT组大鼠上述指标逆转。结论罗格列酮对OLETF大鼠肺组织有抗纤维化作用,可能通过下调TGF-β1/Smad信号转导通路发挥作用。
Objective To investigate the effect and mechanism of rosiglitazone on lung fibrosis in spontaneously diabetic OLETF (Otsuka Long-Evans Tokushima Fatty) rats. Methods Twenty-six male OLETF rats aged 30 weeks were randomly divided into diabetes group (DM group) and rosiglitazone group (RGT group, rosiglitazone 3 mg · kg-1 · d-1 for 12 weeks) The control group was 8 LETO (Long Evans Tokushima Otsuka) rats. The changes of lung tissue structure and collagen deposition were observed by HE and Masson staining. The expressions of Smad3, Smad7 and Collagen Ⅲ in lung tissues were detected by Western blotting. The expressions of TGF-β1 , TGF-β1). Results Compared with the control group, the expression of TGF-β1, Smad3 and type Ⅲ collagen in the lung tissue of DM rats decreased and the expression of Smad7 decreased in the DM group (P <0.05). The collagen deposition in the lung tissue increased Fibrosis trend; Rosiglitazone treatment can make RGT rats reverse the above indicators. Conclusion Rosiglitazone has an anti-fibrotic effect on the lung tissue of OLETF rats, which may play a role by down-regulating TGF-β1 / Smad signaling pathway.