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- 2015-09-16 发布于安徽
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溶酶体酶B抑制剂CA-074Me对病毒性心肌炎小鼠心肌保护作用的研究
张新刚1 赵刚1 李双杰2 李高平1 陈瑞珍1 杨英珍1
1复旦大学医学院附属中山医院,上海市心血管病研究所,上海,2000322湖南省南华大学附属第一医院,湖南衡阳,421001
摘要 目的:观察溶酶体酶B(Cathepsin B)抑制剂CA-074MeCathepsin B蛋白表达水平及血清cTnI明显增加;经CA-074Me干预后,Cathepsin B表达以及cTnI降低,心肌损害减轻,小鼠生存率升高,尤其以H组最明显。结论:CA-074Me通过抑制Cathepsin B关键词Effect of Cathepsin B Inhibitor CA-074Me on the Model of Mice Viral Myocarditis ZHANG Xingang1 Yu Xiaohua2 ZHAO Gang1 LI Shuangjie2, LI Gaoping, CHEN Ruizhen, YANG Yingzhen Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital Fudan University,Shanghai,200032, China 2The First Hospital Attached to Nanhua University in Hunan Province, Hengyang 421001, China
Abstract Objective: To observe the intervention effect of CA-074Me on the model of mouse viral myocarditis, and to explore the possible mechanism of its protection on myocardium. Methods: A total of 55 male 4-week-old BABL/c mice were randomly divided into 4 groups: normal control group (group N, n=10), viral myocarditis group (group V, n=15), CVB3 infected and low dose CA-074Me treated group (group L, n=15) and CVB3 infected and high dose CA074Me treated group (group H, n=15). Every mouse in the experimental group was given 0.1 ml coxsackie B3 virus intraperitoneally . At the same time, 0.1 ml of normal saline was treated in group N. From day 2 to day 8, 0.4mg/kg and 4mg/kg Ca-074Me were given intraperitoneally per day in group L and H mice respectively. On day 15 the serum was collected to detect cardiac troponin I (cTnI), then all of mice were sacrificed and hearts were removed for histologic study on day 15. Results: The cathepsin B expressional levels and serum cTnI levels were
基金项目:国家自然科学基金资助项目(NO
通讯作者 陈瑞珍: chen.ruizhen@zs-hospital.sh.cn
increased remarkably after CVB3 inoculation. In each of CA-074Me treatment groups, cTnI levels were markedly decreased , meanwhile, the myocardial damage was attenuated and mice survival rate was elevated compared with viral myocarditis group, especially high dose CA074M
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