p38激酶途径介导缺氧复合烧伤血清所致乳鼠心肌细胞损害  

p38 kinase pathway mediated cardiomyocyte injury in rats due to hypoxia and burn serum

作　　者：张家平[1] 黄跃生[1] 杨宗城[1] 

机构地区：[1]第三军医大学附属西南医院全军烧伤研究所

出　　处：《第三军医大学学报》2003年第18期1596-1598,共3页Journal of Third Military Medical University

基　　金：国家重点基础研究发展规划资助项目 ("973"项目 ) (G19990 54 2 0 2 ) ;国家杰出青年科学基金资助项目 ( 30 12 50 4 0 ) ;全军"十五"指令性课题 ( 0 1L0 6 6 ) ;教育部高等学校骨干教师资助计划项目 ( 2 0 0 0 ) ;军队首批临床高新技术重大项目 ( 2 0 0

摘　　要：目的　观察缺氧复合烧伤血清对心肌细胞p3 8激酶和JNK活化的影响 ,探讨p3 8激酶在缺氧复合烧伤血清损伤心肌细胞中的作用。方法　免疫印迹化学发光法检测缺氧复合烧伤血清作用培养心肌细胞前后p3 8激酶及JNK磷酸化程度 ,观察p3 8激酶抑制剂SB2 0 3 5 80预先处理 ,对心肌细胞p3 8激酶磷酸化、心肌细胞活力、培养液中LDH活性及凋亡的影响。结果　缺氧复合烧伤血清使心肌细胞p3 8激酶迅速、持续活化 ,而JNK活化不明显 ;10 μmol LSB2 0 3 5 80可有效抑制p3 8激酶活化 ,并显著降低细胞培养液中LDH活性及细胞凋亡率 ,改善心肌细胞活力。结论　MAPKs家族两条应激活化的信号途径当中 ,p3 8激酶途径是缺氧复合烧伤血清作用条件下心肌细胞主要被激活途径 。Objective To investigate the roles of the activated p38 kinase in cell injury by observation of the effects of hypoxia and burn serum on cardiomyocyte p38 kinase and JNK activation. Methods Phosphorylation of p38 kinase and JNK in primary cultured neonatal rat cardiomyocytes before and after hypoxia and burn serum was determined by Western blotting. Effects of pretreatment with SB203580 at the dose of 10 μmol/L on the changes of phosphorylation of p38 kinase in cardiomyocytes, lactate dehydrogenase (LDH) activity, cell vitality and apoptosis were investigated, respectively. Results Exposure of rat neonatal cardiomyocytes to hypoxia and burn serum resulted in a rapid and long lasting activation of p38 kinase but no significant activation of JNK. SB203580(10 μmol/l), a selective inhibitor of p38 kinase, could inhibit p38 kinase activation dramatically, decrease the LDH activity in culture media and cell apoptosis significantly and improve cell vitality. Conclusion In the two stress activated signal pathways of MAPKs family, p38 kinase pathway, but not JNK, is the major pathway activated by hypoxia and burn serum and participates in the cardiomyocyte injury.

关 键 词：心肌细胞 蛋白激酶p38 缺氧 烧伤血清 

分 类 号：R322.11[医药卫生—人体解剖和组织胚胎学] R644.02[医药卫生—基础医学]