摘要
目的探讨吸烟诱导肺气肿大鼠血清抗血管内皮细胞抗体(AECA)的表达,分析甲基波尼松龙对其干预影响。方法将39只大鼠随机分为对照组、吸烟大鼠肺气肿模型组(模型组)、甲基波尼松龙干预组(干预组)。模型组及干预组进行烟雾暴露被动吸烟1个月时,对干预组腹腔注射甲基波尼松龙(每天1次,每周6d)。烟雾暴露90d后,比较各组大鼠血清AECA、支气管肺泡灌洗液(BACF)中白细胞介素-8(IL-8)、基质金属蛋白酶-9(MMP-9)、肿瘤坏死因子-α(TNF-α)及肺组织中肺平均内衬间隔(MLI)、平均肺泡数(MAN)的差异。结果模型组血清AECA比对照组、干预组升高(P<0.05);模型组BALF中IL-8、TNF-α、MMP-9水平较对照组、干预组均升高(P<0.05)。结论 AECA参与吸烟诱导肺气肿大鼠形成,甲基波尼松龙可降低AECA及细胞炎症因子水平,并影响肺气肿的形成。
Objective To investigate the expression of anti-endothelial cell antibody AECA in the emphysema rats induced by smoking and to analyze the intervention effect of methylprednisolone on it.Methods Thirty-nine rats were randomly divided into the control group,smoking rat emphysema model group(model group)and methylprednisolone intervention group(intervention group).The model group and intervention group conducted the 1-month passive smoking by smog exposure.The intervention group was intraperitoneally injected by methylprednisolone(once daily,6dper week).After exposing to smog for 90 d,the differences of serum AECA level,IL-8,MMP-9and TNF-αlevel in bronchoalveolar lavage fluid(BALF),lung MLI and mean alveolar number(MAN)were compared among groups.Results Compared with the control group and theintervention group,the level of serum AECA in the model group was significantly increased(P〈0.05);Compared with the control group and intervention group,the IL-8,TNF-αand MMP-9levels of BALF in the model group were also increased(P〈0.05).Conclusion ACEA participates in the smoking induced emphysema formation;methylprednisolone may decrease the level of AECA and cell inflammatory factors and affects the emphysema formation.
作者
张璐
王中新
马丽
张程
张湘燕
Zhang Lu Wang Zhongxin Ma LiA Zhang Cheng Zhang Xiangyan(Department of Respiratory and Critical Care Medicine, Guizhou Provincial People's Hospital, Gui yang , Guizhou 550002, Chin)
出处
《重庆医学》
CAS
北大核心
2017年第9期1156-1158,共3页
Chongqing medicine
基金
国家自然科学基金资助项目(81060006)
十二五国家科技支撑计划课题资助项目(2013bai09b09)
贵州省科学技术基金资助项目[黔科合j字(2011)2251]