山东医药2011，Vol.51Issue(21)：10-12,3.
过氧化物酶体增殖物激活受体γ及其配体调节大鼠肺纤维化的作用机制
Molecular mechanism of peroxisome proliferator activated receptor gamma and its agonist on bleomycin-induced pulmonary fibrosis in rats
摘要
Abstract
Objective To investigate the influence and mechanism of PPAR γ and its agonist on bleomycin-induced pulmonary fibrosis in rats. Methods Twenty-four male SD rate were randomly divided into 4 groups, ie. saline control group, rosiglitazone control group, bleomycin group, treatment group of resiglitazone. The model of pulmonary fibrosis induced by intracheel bleomycin. The morphological changes of lung tissue were obnerved by masson staining. The hydroxyproline levels of lung tissue were detected. Expreesions of MMP-9, TGF-β1 and PPARγ were measured by real time RT-PCR and inununohistochemistry. Results The collagen deposition, the hydroxyproline levels of lung tissue, the expressions of TGF-β1, MMP-9 and PPARγ were increased in the bleomycin group compared to the saline group (P ＜0.05 ); the other indexes were decreased in the rosiglitazone treatment group compared to the Bleomycin group, except that the expression of PPARγwas significantly increased ( P ＜0. 05). The protein expression of PPARγwas negatively correlated with the expressions of TGF-β1 mRNA and MMP-9 mRNA ( all P ＜0.05). Conclusions PPARγ involves in pulmonary fibrosis induced by bleomycin. Rosiglitazone can alleviate pulmonary fibrosis through inhibition of TGF-β1 and MMP-9 transcription.关键词
过氧化物酶体增殖物激活受体γ/罗格列酮/博莱霉素/肺/大鼠Key words
peroxisome proliferator activated receptor gamma/ resiglitazone/ bleomycin/ pulmonary fibrsis分类
医药卫生引用本文复制引用
刘维佳,刘琳,张湘燕,饶珊珊..过氧化物酶体增殖物激活受体γ及其配体调节大鼠肺纤维化的作用机制[J].山东医药,2011,51(21):10-12,3.基金项目
贵州省科学技术基金项目(黔科合J字20082182号) （黔科合J字20082182号）
贵州省优秀科技教育人才省长专项资金项目(黔省专合字200762号). （黔省专合字200762号）
