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作 者:范鹏举[1] 黄跃生[1] 黄晓元[2] 郑军[1]
机构地区:[1]第三军医大学西南医院全军烧伤研究所 [2]中南大学湘雅医院烧伤整形外科,长沙430008
出 处:《第三军医大学学报》2004年第23期2089-2092,共4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)(G1999054205);国家杰出青年科学基金资助项目(30125040)~~
摘 要:目的 构建严重烧伤后合并心肌负荷增加的体外心肌细胞模型 ,探讨p3 8、JNK、c jun、ATF 2的活化情况 ,明确高机械牵张刺激对严重烧伤后心肌细胞损伤信号的传导。方法 采用原代培养的乳鼠心肌细胞 ,分别给予正常血清(SN组 )、烧伤血清 +缺氧 (1%O2 ) (SH组 )、烧伤血清 +缺氧 (1%O2 ) + 10 %轴向静态牵张 (SHS组 ) 3种处理 ,采用Westernbloting检测磷酸化p3 8、JNK、c jun、ATF 2水平。结果 施加缺氧复合烧伤血清刺激后 ,磷酸化p3 8、c jun、ATF 2水平升高。在施加高机械牵张后p3 8升高更加明显 ,而后两者与前者表现相反。JNK自始至终没有出现活化。结论 严重烧伤后 ,p3 8可能是介导心肌细胞损伤的重要信号传导分子 ,而JNK并未参与严重烧伤后心肌细胞损伤的信号传导 ,转录因子c jun、ATF2亦可能参与严重烧伤后心肌细胞的损伤 ,但在严重烧伤合并心脏负荷增加的情况下可能并不是主要的调控因子。Objective To investigate the activation of p38, JNK, c-jun, and ATF2 by high stretch in cardiomyocytes after severe burn and to understand the signal transduction through which the high stretch injuries cardiomyocyte after the severe burn. Methods Ventricular cardiac myocytes isolated from neonatal rats were employed in this study. The cells were stimulated by sera of normal rats (SN group), burn sera and hypoxia (SH group), burn sera and hypoxia and 10% axial static stretch (SHS group), respectively. Activation of p38, JNK, c-jun, and ATF2 in cardiomyocytes was determined by Western bloting. Results The activation of p38, c-jun, and ATF2 in SH group and SHS group increased as compared with that in SN group. High stretch on cardiomyocytes under burn sera and hypoxia induced significant increase of p38, but the latter two were different from the former one. JNK was not activated by the two stimuli. Conclusion After severe burn, p38 may be the important signal transducer in cardiomyocytes, but JNK may not take part in this signal transduction. C-jun and ATF2 may contribute to cardiomyocyte damage after sever burn, but they may not be the main regulatory factors after severe burn combined with the increase of heart load.
分 类 号:R322.11[医药卫生—人体解剖和组织胚胎学] R363.11[医药卫生—基础医学]
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