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烫伤大鼠心肌细胞丝裂素活化蛋白激酶的活化及胞内分布规律的研究
引用本文:张家平,黄跃生,刘敬,周新,罗中华.烫伤大鼠心肌细胞丝裂素活化蛋白激酶的活化及胞内分布规律的研究[J].中华烧伤杂志,2003,19(3):137-140.
作者姓名:张家平  黄跃生  刘敬  周新  罗中华
作者单位:400038,重庆,第三军医大学西南医院全军烧伤研究所
基金项目:国家杰出青年科学基金资助项目 (3 0 12 5 0 40 ),国家重点基础研究发展规划资助项目 (G19990 5 42 0 2 ),军队医药卫生科研基金“十五”重点课题 (0 1L0 66),全国高等学校骨干教师资助项目
摘    要:目的 观察大鼠严重烫伤后早期心肌细胞中丝裂素活化蛋白激酶 MAPKs,包括 p38激酶、细胞外信号调节激酶 (ERKs)和应激活化蛋白激酶 (JNK) ]的活化及胞内分布规律 ,探讨其与心肌损伤的关系。 方法 制作严重烫伤大鼠模型 ,于伤后 1、3、6、12、2 4h取其全血及心肌组织标本 ,并取正常大鼠的相应标本为对照。常规检测各血清标本中肌酸激酶同工酶 MB(CK MB)的活力 ;采用Western印迹法 ,检测各心肌组织标本中MAPKs各成员的活化情况 ,并对其组织切片行免疫组化染色。 结果 伤后 p38激酶、ERK均发生活化并伴核转位 ,以 1、3、6h最明显 (P <0 .0 1) ;伤后 1~ 2 4hJNK均未见活化。血清CK MB含量于伤后 3h升高 ,12h达高峰 (P <0 .0 5~ 0 .0 1)。 结论 p38激酶和ERK信号通路可能在严重烧伤后早期心肌细胞发生的损伤性反应中起重要作用 ,而前者可能是烧伤引发心肌损伤的主要信号转导通路之一。

关 键 词:烫伤  大鼠  心肌细胞  丝裂素活化蛋白激酶  活化  胞内分布规律  研究  烧伤  信号转导
修稿时间:2002年5月8日

An experimental study of the intracellular distribution and the activation of mitogen-activated protein kinases in myocardial cells in scalded rats
ZHANG Jia-ping,HUANG Yue-sheng,LIU Jing,ZHOU Xin,LUO Zhong-hua.An experimental study of the intracellular distribution and the activation of mitogen-activated protein kinases in myocardial cells in scalded rats[J].Chinese Journal of Burns,2003,19(3):137-140.
Authors:ZHANG Jia-ping  HUANG Yue-sheng  LIU Jing  ZHOU Xin  LUO Zhong-hua
Institution:Institute of Burn Research, Southwest Hospital, The Third Military Medical University, Chongqing, PR China.
Abstract:OBJECTIVE: To investigate the intracellular distribution and the activation of mitogen-activated protein kinases (MAPKs) in myocardial cells in scalded rats. METHODS: Wistar rats were used in this study and forty of them were inflicted with 40% III degree scald on the back and eight normal ones as control. The samples of plasma and myocardial tissue were harvested at 1, 3, 6, 12 and 24 postburn hours (PBHs), and samples were also obtained from normal rats as control. The plasma CK-MB activity was determined by routine method. The activation states of all the members of MAPKs p38 kinase, ERKs (extracellular signal-regulated protein kinases) and JNK (c-Jun N-terminal kinase)] in the myocardial tissue samples were detected by Western blotting. The tissue slides were stained by immunohistochemistry methods. RESULTS: Activation of p38 kinase and ERK with nuclear translocation was found postburn, especially during 1, 3 and 6 PBHs (P < 0.01). But there was no activation of JNK during 1 - 24 PBHs. The plasma CK-MB content increased at 3 PBH and reached summit at 12 PBHs (P < 0.05 - 0.01). CONCLUSION: p38 kinase and ERK signal pathways might play important roles in the early postburn injury of myocardial cells, inducing myocardial injury.
Keywords:Myocardium  Mitogen-activated protein kinase  Burn  Signal transduction
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