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吡格列酮对大鼠心肌缺血再灌注损伤中炎症反应及细胞凋亡的影响

Effect of pioglitazone on inflammatory reaction and apoptosis of myocardium cell from ischemia-reperfusion injury in rats
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摘要 目的探讨吡格列酮对大鼠心肌缺血再灌注损伤中炎症反应和细胞凋亡的影响及其机制。方法将80只SD大鼠随机分为假手术组、模型组、吡格列酮组、GW9662组及DMSO组,每组各16只,术前5 d分别给予相应处理。采取体内结扎左前降支的方法建立心肌缺血再灌注损伤模型,予ELISA法检测大鼠心肌组织中NF-κB p65及IFN-γ含量水平,HE染色观察左心室前壁细胞病理形态学改变,并采用原位末端标记法检测心肌细胞凋亡数。结果与假手术组相比,其余四组大鼠心肌组织中NF-κB p65及IFN-γ含量水平、心肌细胞凋亡数均显著升高(P<0.05);与模型组比较,吡格列酮组大鼠心肌组织中NF-κB p65及IFN-γ含量水平,心肌细胞凋亡数明显降低(P<0.05);模型组与吡格列酮组中NF-κB p65及IFN-γ含量水平均呈显著正相关(P<0.001)。结论吡格列酮在心肌缺血再灌注损伤中可能通过负性调节NF-κB p65含量水平进而减少IFN-γ的释放,抑制心肌细胞的凋亡,从而发挥相应的心肌保护作用。 Objective To investigate the effect of pioglitazone on inflammatory reaction and apoptosis of neurons following myocardium from ischemia-reperfusion injury in rats and its corresponding mechanisms. Methods Eighty Spragne-Dawley rats were randomly divided into five groups as sham-operation group, model group, pioglitazone group, GW9662 group and DMSO group, with 16 rats in each group. Relevant treatments were given to rats 5 days before myocardium iscbemia operation respectively. A rat model of left anterior descending coro- nary artery was ligated for 45 rain and reperfused for 45 rain to establish the model of ischemia-reperfusion. ELISA was respectively used to detect levels of NF-rB p65 and IFN-T in myocardium tissue. H.E staining was employed to observe morphologic changes of myocardium cells in iscbemia/reperfusion injury region, and TUNEL staining were used to detect the number of myocardium cell apoptosis. Results Compared with sham-operation group, the levels of NF--KB p65 and IFN-y, the number of myocardium cell apoptosis were significantly increased in the other four groups (P〈0.05); compared with model group, the levels of NF-r.B p65 and IFN-T, the number of myocardium apop- tosis were significantly decreased in pioglitazone group (P〈0.05). The levels of IFN-y and NF-I〈B p65 in model group and pioglitazone group had perfect positive correlation (P〈0.001). Conclusion Pioglitazone maybe down-reg- ulates NF-kB p65 level and reduces the release of IFN-T, then prevents cell apoptosis, and hence provides protection from ischemia/reperfusion injury.
出处 《海南医学》 CAS 2013年第24期3595-3598,共4页 Hainan Medical Journal
关键词 吡格列酮 GW9662 心肌缺血 再灌注 炎症反应 细胞凋亡 Pioglitazone GW9662 Myocardium ischemia/reperfusion Inflammatory response Cell apoptosis
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