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作 者:沈诚[1] 范士志[1] 陈建明[1] 李志平[1] 何勇[1]
机构地区:[1]第三军医大学大坪医院野战外科研究所全军胸心外科中心,重庆400042
出 处:《重庆医学》2006年第1期38-39,共2页Chongqing medicine
摘 要:目的研究抑制Janus激酶/信号转导和转录激活子(JAK/STAT,janus kinase/signal transducer and activator oftranscription)通路对缺血再灌注损伤时大鼠心肌组织TNF-α和IL-6表达的影响。方法采用离体工作心脏灌注模型,大鼠随机分为正常对照组,缺血再灌注组,JAK抑制剂-AG490治疗组,STAT抑制剂-RMP治疗组。采用ELISA检测试剂盒检测TNF-α和IL-6含量。结果与正常对照组相比,心肌组织TNF-α和IL-6含量在缺血再灌注后有显著性增加(P<0.01)。AG490及RMP处理后,TNF-α和IL-6含量与缺血再灌注组相比有明显下降(P<0.01);与正常对照组相比较,仅有少许升高,差异无统计学意义(P>0.05)。TNF-α含量增加时IL-6含量也相应升高,反之亦相同,两者呈一定程度的正相关。结论心肌缺血再灌注损伤使TNF-α和IL-6表达明显升高,抑制JAK/STAT通路的活化可下调心肌组织TNF-α和IL-6的表达,这可能有助于减轻缺血再灌注所致心肌损伤,并抑制急性炎症反应的发生。Objective To investigate the effect of inhibitors of janus kinase /signal transducer and activator ot transeription (JAK/STAT) pathway in mediating level of TNF-α and IL-6 in rat cardial muscles during ischemia-reperfusion. Methods Twentyfour male SD rats for isolated rat heart model were randomly divided into control group(n= 6), ischemia-reperfusion group(n= 6), AG490 treatment group(n= 6), RMP treatment group(n= 6). Level of TNF-α and IL-6 in the myocardium were measured by enzyme-linked immunosorbent assay(ELISA) system. Results TNF-α and IL-6 levels significantly increased after ischemia-reperfusion(P〈0.01). The levels of TNF-α and IL6 in AG490 or RMP treatment groups were significantly lower than that in ischemiareperfusion group (P〈0.01), The levels of TNF-α and 1L-6 in AG490 or RMP treatment groups were little higher than that in control group,but there were no significantly changes between the two groups(P〉0.05). Conelusion The result suggest that myocardial ischemia-reperfusion can result in intensive activation of TNF-α and IL-6. Early treatment with inhibitors to JAK/STAT pathway might he benefit for attenuation of myocardial injury induced by ischemia-reperfusion and subsequent acute inflammatory response.
关 键 词:JAK/STAT通路 缺血再灌注 TNF-Α IL-6
分 类 号:R541[医药卫生—心血管疾病]
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