大鼠心肌缺血缺氧损伤核转录因子-κB与细胞间粘附分子-1的表达  

Expression of nuclear transcription factor -κB and intercellular adhesion molecule-1 in myocardial injury rats

作　　者：金戈[1] 陈珊[2] 单江[2] 许励[3] 张梅[3] 茹国庆[3] 

机构地区：[1]浙江省人民医院临床药理室,浙江杭州310014 [2]浙江大学医学院附属二院心内科 [3]浙江省人民医院病理科

出　　处：《毒理学杂志》2005年第2期120-122,共3页Journal of Toxicology

摘　　要：目的　研究异丙肾上腺素致大鼠心肌损伤对心肌核转录因子 κB(NF κB)以及细胞间粘附分子 1(ICAM 1)表达的影响。方法　大鼠皮下注射异丙肾上腺素造成心肌坏死模型,测定血清乳酸脱氢酶(LDH)、肌酸磷酸激酶(CK)活力和丙二醛(MDA)含量,观察心肌坏死程度,免疫组化检测心肌NF κBp65蛋白的表达,Western蛋白质印迹杂交检测IκBα的蛋白质表达,半定量RT PCR检测ICAM 1mRNA含量。观察腹腔注射地塞米松后上述指标的变化。结果　大鼠给予异丙肾上腺素后,血清LDH、CK和MDA含量升高,心肌坏死,NF κBp65蛋白大量表达,IκBα蛋白质表达减弱,ICAM 1mRNA表达上升。地塞米松使升高的LDH、CK和MDA明显下降,减轻心肌坏死程度,显著抑制NF κBp65蛋白和ICAM 1mRNA表达,IκBα蛋白质表达增强。结论　儿茶酚胺大量释放引起的心肌缺血缺氧损伤中,NF κB和ICAM 1mRNA表达增加,表明抑制NF κB激活,减少ICAM 1mRNA的表达及炎性细胞因子产生是减少心肌缺血缺氧损伤的关键点之一。Objective To investigate influence on myocardial nuclear transcription factor-κB (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) expression during myocardial injury induced by isoproterenol in rats.Method Induced myocardial ischaemia and anoxia in rats by injected isoproterenol,detected serum activity of lactate dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA), evaluated NF-κB p65 protein expression by immunohistochemical analysis, detected activity of IκBα by western blotting, measured expression of ICAM-1 mRNA by RT-PCR. Observe changes of these parameters after treated with dexamethasone.Results Isoproterenol increased serum level of LDH,CK,MDA,resulted in myocardial necrosis, activated NF-κB p65 and ICAM-1 expression and Inhibited IκBα activity. Dexamethasone attenuated these changes.Conclusion Isoproterenol has myocardial toxic effect in rats by upregulating NF-κB protein and ICAM-1 mRNA expression. Inhibiting NF-κB activity and attenuating ICAM-1 expression are key points to protect myocardial injuries.

关 键 词：细胞间粘附分子-1 核转录因子-ΚB 缺氧损伤 心肌缺血 大鼠 ICAM-1 定量RT-PCR检测 异丙肾上腺素 丙二醛(MDA) mRNA表达 P65蛋白 血清乳酸脱氢酶 Western NF-ΚB激活 蛋白质表达 心肌坏死 肌酸磷酸激酶 免疫组化检测 IκBα 

分 类 号：R285.5[医药卫生—中药学] R692[医药卫生—中医学]