肺纤维化中过氧化物酶体增殖物激活受体γ的参与机制研究

肺纤维化中过氧化物酶体增殖物激活受体γ的参与机制研究刘维佳;韩婧;张湘燕;李万成
【期刊名称】《广东医学》
【年(卷),期】2011(32)14
【摘要】Objective To investigate the roles of peroxisome proliferator activated receptor - gamma ( PPARγ )and its agonist in bleomycin -induced pulmonary fibrosis in rats. Methods Twenty - four male SD rats were randomly divided into 4 groups: saline control group, rosiglitazone control group, bleomycin group and rosiglitazone treatment group. Pulmonary fibrosis model was induced by intra - tracheal injection of bleomycin. The morphological changes of lung tissue were observed by HE and Masson staining. The levels of LDH and TGF - β1 in BALF were measured. Expression of TGF - β1 and PPARγ in lung tissue was quantified time RT - PCR and Western blot. Results Increases of Ashcroft score, collagen deposition, expression of TGF - β1 and PPARγ , and levels of LDH and TGF - β1 in BALF were revealed in bleomycin group, when compared to those in saline group. Except for the expression of PPARγ, the other indexes were reduced in rosiglitazone treatment group, when compared to those in bleomycin group. Moreover, the expression of PPARγ was negatively correlated with the expression of TGF - β1 mRNA and the level of LDH in BALF in bleomycin group. Conclusion PPAR.γ is involved in pulmo nary fibrosis induced by bleomycin. PPARγ and its ligand
rosiglitazone inhibit pulmonary fibrosis, via regulating inflammation and down - regulating TGF - β1 transcription.%目的探讨过氧化物酶体增殖物激活受体γ(PPARγ)及其配体在博莱霉素诱导大鼠肺纤维化中的作用及参与机制.方法将24只雄性SD大鼠随机分为生理盐水对照组、罗格列酮对照组、博莱霉素组、罗格列酮干预组.经气管内注射博莱霉素建立肺纤维化模型.HE染色及Masson染色观察肺组织形态学变化,检测支气管肺泡灌洗液(BALF)中乳酸脱氢酶(LDH)及转化生长因子β1(TGF-β1)浓度,应用荧光定量RT-PCR及Wes tern blot检测肺组织中TGF-β1和PPARγ表达.结果博莱霉素气管内注入后肺Ashcroft评分、胶原沉积、TGF-β1表达、PPARγ表达及BALF中LDH、TGF-β1水平增加;给予罗格列酮干预后,除PPARγ表达进一步增加外,上述指标均下降.博莱霉素组PPARγ蛋白水平与TGF-β1 mRNA表达、BALF中LDH含量呈负相关.结论PPARγ参与了肺纤维化的发生;PPARγ及其配体罗格列酮可能通过调节炎症反应,抑制TGF-β1转录,从而减少胶原沉积,对肺纤维化进行负性调控.
【总页数】4页(P1796-1799)
【作者】刘维佳;韩婧;张湘燕;李万成
【作者单位】贵州省人民医院呼吸内科,贵阳550002;贵州省人民医院呼吸内科,贵阳550002;贵州省人民医院呼吸内科,贵阳550002;成都医学院第一附属医院呼吸内科,成都,610500
【正文语种】中文
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