急性肺损伤大鼠肺组织PPAR-γ表达的研究  

PPARγ expressions in rat lung tissues after acute lung injury

作　　者：王建春[1] 姜鹏[2] 黄建 钱桂生[1] 

机构地区：[1]第三军医大学新桥医院全军呼吸内科研究所,全军呼吸病研究重点实验室,重庆400037 [2]兰州军区乌鲁木齐总医院呼吸科,乌鲁木齐830000 [3]重庆武警医院呼吸科,重庆400061

出　　处：《第三军医大学学报》2008年第6期468-471,共4页Journal of Third Military Medical University

基　　金：国家自然科学基金(30570808);全军医学科研“十一五”科技攻关项目(06G083)~~

摘　　要：目的在脂多糖(lipopolysaccharide,LPS)复制的急性肺损伤(acute lung injury,ALI)大鼠模型中,观察PPARγ表达的改变,探讨PPAR-γ在ALI发病中的作用。方法在LPS复制的大鼠ALI模型中,观察动脉血气、肺湿/干(W/D)比值、肺组织病理,用RT-PCR法检测肺组织PPAR-γ、TNF-α mRNA表达,用ELISA法检测TNF-α蛋白变化,并用免疫组化观察肺组织PPAR-γ的改变。结果ALI大鼠,PaO2显著降低(P<0·05),肺W/D比值显著高于对照组(P<0·05),病理显示肺组织受损;肺组织TNF-α mRNA显著升高(P<0·05),与此同时血浆TNF-α亦显著升高(P<0·05)。正常大鼠肺组织可表达PPAR-γ,LPS致伤后肺组织PPAR-γ mRNA在1h即开始下降,2h降至谷底,并持续至实验结束。免疫组化显示致伤后1、2h与对照组无显著差异,从4h显著降低并持续至8h(P<0·05)。结论正常大鼠肺组织可表达PPAR-γ,LPS可引起ALI大鼠肺组织PPAR-γ的基因和蛋白水平表达下降,这可能与ALI炎症持续和损伤有关。Objective To observe the changes of PPARγ expressions in acute lung injury （ALI） rats and explore the role of PPARγ in the pathogenesis of ALI. Methods ALI model was induced by lipopolysaccharide （LPS） in 32 male Wistar rats. Another 8 matched normal rats were used as control. At 1,2, 4, 8 h after ALI, arterial blood gas analysis, lung tissue wet/dry weight ratio, lung histopathological changes were observed; The expressions of PPARγ/and TNF-α mRNA were detected by RT-PCR; TNF-α content was examined with ELISA; PPARγ/protein in lung tissues was detected by immunohistochemistry. Results Compared with control rats, PaO2 of ALl rats decreased significantly （ P 〈 0. 05 ） ; Lung wet/dry weight ratio rose （ P 〈 0. 05 ） ; Lung tissues were damaged histopathologically; The expressions of TNF-α mRNA in lung tissues and blood plasma increased markedly （ P 〈 0. 05 ）. PPARγ/expressed in lung tissues of control rats. PPARγ/mRNA expressions in lung tissues decreased in 1 h after ALl, declined to the lowest level 2 h after ALI and kept at a low level to the end of observation peroid. Immunohistochemical staining of PPARγ showed that there was no difference between ALl rats and control rats at 1 h and 2 h after ALl, and significant decrease occurred 4 h after ALl and lasted to 8 h after ALl （P 〈 0. 05 ）. Conclusion Lung tissues of normal rats express PPARγ. The decreased PPARγ/mRNA and protein expressions in the rats of ALl caused by LPS may be associated with inflammation and damage of lung tissues.

关 键 词：过氧化物酶增殖体激活受体-γ(PPAR-γ) 急性肺损伤(ALI) 脂多糖(LPS) 

分 类 号：R322.35[医药卫生—人体解剖和组织胚胎学] R394.2[医药卫生—基础医学]