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机构地区:[1]吉林大学第二医院心血管内科,吉林长春130041 [2]白城市医院骨外科,吉林白城137000
出 处:《诊断学理论与实践》2008年第3期323-325,共3页Journal of Diagnostics Concepts & Practice
基 金:长春市科技厅资助课题(编号:06GG31)
摘 要:目的:观察左旋卡尼汀(肉碱)及盐酸曲美他嗪(万爽力)对异丙肾上腺素所致大鼠心肌细胞凋亡的影响。方法:将60只SD大鼠随机分成3组,对照组、肉碱组、万爽力组,每组各20只。肉碱组大鼠每只予肉碱200 mg/(kg·d)腹腔注射,每日1次,连用42 d;万爽力组大鼠每只予万爽力5 mg/(kg·d)腹腔注射,每日1次,连用42 d;对照组大鼠在另2组使用肉碱、盐酸曲美他嗪时以等量的生理盐水腹腔注射。所有大鼠在第43天、44天后均予异丙肾上腺素制造心肌缺血模型,观察心肌细胞凋亡相关蛋白Bcl-2及Caspase-3的表达及病理损害程度。结果:肉碱组Bcl-2蛋白阳性表达指数高于万爽力组;肉碱组和万爽力组Bcl-2蛋白阳性表达指数高于对照组:肉碱组Caspase-3蛋白阳性表达指数低于万爽力组;肉碱组和万爽力组Caspase-3蛋白阳性表达指数低于对照组,所有差异均有统计学意义(P均<0.05)。肉碱组及万爽力组病理检查见大部分病灶组织为小灶性坏死;对照组的坏死灶已融合,心肌损伤明显加重。结论:肉碱在异丙肾上腺素所致的心肌缺血模型上具抗缺血、缺氧损伤作用,与盐酸曲美他嗪相比对缺血心肌有更明显的保护作用,其机制可能是通过调节Bcl-2和Caspase-3介导的细胞凋亡实现。.Objective To investigate the effect of L-carnitine and trimetazidine hydrochloride on cardiomyocyte apoptosis induced by isoproterenol in rats. Methods Sixty SD rats were randomly divided into three groups: control group (n=20), L-camithine group (n=20) and trimetazidine hydrochlofide group (n=20), Isoproterenol was used to induce myocardial ischemia in all the groups and the expressions of Bcl-2 and Caspase-3 and degree of pathological lesion were examined. Results The expression of Bcl-2 in L-earnitine group was significantly higher than that in tfimetazidine hydrochloride group (P〈0.05) and both were significantly higher than that in control group (P〈0.05). Expression of easpase- 3 in L-carnithine group was significantly lower than that in trimetazidine hydroehloride group (P〈0.05) and both were significantly lower than that in control group (P〈0.05). Histological examination showed that most of the lesions in L- camithine and trimetazidine hvdroehlofide groups were small focal necrosis whereas that in control group were confluent necrotic lesions, significantly more severe. Conclusions In rats with isoproterenol induced myocardial isehemia, Lcarnitine had protective effect against ischemic and anoxic injuries and its protective activity was higher than that of trimetazidine hydrochloride. The mechanism of this protective action might be through the modulation of apoptosis via the expressions of Bcl-2 and Caspase-3.
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