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作 者:钱文浩[1] 李东野[1] 於江泉[1] 张中明[2] 孙全胜[2] 董红燕[3]
机构地区:[1]徐州医学院附属医院心内科,江苏徐州221000 [2]徐州医学院附属医院胸心外科 [3]徐州医学院神经生物学研究中心
出 处:《临床心血管病杂志》2008年第3期210-212,共3页Journal of Clinical Cardiology
基 金:江苏省卫生厅资助项目(No:H200329)
摘 要:目的:探讨冠心病患者冬眠心肌细胞内活化的丝裂素活化蛋白激酶(p38MAPK)对心肌细胞凋亡的影响。方法:行冠状动脉搭桥术(CABG)的冠心病患者10例,术前1周内用多巴酚丁胺超声负荷试验结合多普勒组织成像确定冬眠心肌及正常心肌的存在部位,CABG术中根据检测结果进行取材(分别取正常心肌和冬眠心肌),并经电镜证实。取材心肌用Tunel法检测心肌细胞凋亡情况,免疫印迹法(Western-blot)检测磷酸化的p38的表达情况。结果:冬眠心肌细胞内磷酸化p38、心肌细胞凋亡数较正常心肌高;p38与心肌细胞凋亡数相关(P<0.05,r=0.816)。结论:心肌慢性缺血时,心肌细胞内p38MAPK信号活化,活化的p38MAPK介导冬眠心肌细胞凋亡。Objective:To observe the relationship of p38MAPK and cardiomyocyte apoptosis in hibernating myocardium(HM) in patients with coronary artery disease (CAD). Method:Ten patients with CAD scheduled for bypass surgery underwent preoperative dobutamine stress echocardiography (DSE), doppler tissue image (DTI) to check the position of HM and intraoperative myocardial biopsies. The normal myocardium and the HM were obtained during operation. They were conformed by electron microscope. Cardiomyocyte apoptosis were detected by Tunel, and P-P38 were detected by Western-blot method. Result: P-P38 and PCN of apoptosis were significantly increased in CHM compared with normal myocardium. P-P38 and PCN of apoptosis were positive correlation in hibernating myocardium (r= 0. 816 P〈0.05). Conclusion: p38MAPK triggered by ischemia could intervene cardiomyocyte apoptosis.
关 键 词:冠状动脉疾病 冬眠心肌 P38丝裂素活化蛋白激酶 细胞凋亡
分 类 号:R541.4[医药卫生—心血管疾病] R540[医药卫生—内科学]
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