摘要
目的:观察内质网应激标志蛋白GRP78和氧化应激指标在博来霉素诱导的肺纤维化中的变化及中药丹芍化纤胶囊对它的影响。方法:选取SD大鼠30只,随机分为正常对照组(正常组)、肺纤维化模型组(模型组)和丹芍化纤胶囊治疗组(丹芍组),每组各10只。正常对照组气管内滴注生理盐水,模型组和丹芍组气管内一次性灌注博来霉素5 mg/kg诱导肺纤维化,丹芍组于造模第2天给予丹芍化纤胶囊混悬液灌胃0.8 g/(kg.d)治疗,正常组及模型组则给予等量生理盐水灌胃。实验第28天称大鼠体重,处死各组大鼠,称肺湿重并收集肺组织,行HE和Masson染色观察肺组织病理变化;比色法检测肺组织MDA及SOD变化;采用免疫组织化学方法检测肺组织中GRP78蛋白的表达情况。结果:①与正常组比较,模型组大鼠肺组织中MDA含量及GRP78表达明显升高,而SOD酶活性则显著下降。②与模型组比较,丹芍组大鼠肺组织中MDA含量及GRP78蛋白表达明显降低,但仍较正常组高;SOD酶活性显著回升,但未恢复正常水平。结论:丹芍化纤胶囊可在一定程度上减轻博来霉素诱导的肺泡炎症反应及肺纤维化进展,对肺纤维化具有一定的治疗作用。丹芍化纤胶囊对肺纤维化的干预机制可能与丹芍化纤胶囊提高肺组织SOD酶活性,对抗氧化应激以及抑制肺组织中GRP78的表达,减轻内质网应激反应有关。
Objective：To investigate the effect of endoplasmic reticulum stress and oxidative stress in bleomycin-induced pulmonary fibrosis and protective effect of Danshaohuaxian（DSHX） capsule in this model.Methods：Thirty SD rats were randomly divided into normal control group,pulmonary fibrosis model group and DSHX capsule therapeutic group.Pulmonary fibrosis model was induced by intratracheal instillation of single dose of bleomycin 5 mg/kg.DSHX capsule 0.8 g/kg was administered daily by oral in the therapeutic groups on the second day after bleomycin.All rats were killed on the 28th day.The levels of MDA and SOD,and the expression of GRP78 in pulmonary tissue were detected.Results：Compared with the control group,the levels of MDA and GRP78 in model group were increased,while the activity of SOD was decreased.After the treatment of DSHX capsule,the levels of MDA and GRP78 were decreased,while the activity of SOD was elevated.Conclusion：DSHC capsule can reduce pulmonary alveolus inflammation and pulmonary fibrosis induced by bleomycin,the mechanisms of which may be the elevation of the activity of SOD in lung tissue to alleviate oxidative stress and endoplasmic reticulum stress.
出处
《重庆医科大学学报》
CAS
CSCD
北大核心
2011年第7期805-808,共4页
Journal of Chongqing Medical University
基金
贵州省科技攻关资助项目(编号:黔科合SZ字[2008]3049号)
贵州省科技厅国际科技合作项目(编号:黔科合外G字[2010]7016号)
关键词
肺纤维化
丹芍化纤胶囊
内质网应激
氧化应激
pulmonary fibrosis
danshaohuaxian capsule
endoplasmic reticulum stress
oxidative stress
作者简介
谢汝佳（1979-），女，讲师，硕士，研究方向：肝纤维化发病机制研究。
通信作者：杨勤，女，教授，Email：qinyang@gmc．edu．cn。
