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作 者:林高翔[1] 梅胜兰[2] 谭永星[1] 庞宏宣[1]
机构地区:[1]桂林医学院附属医院麻醉科,541004 [2]桂林医学院研究生学院
出 处:《中华麻醉学杂志》2012年第2期218-220,共3页Chinese Journal of Anesthesiology
基 金:广西卫生厅科研基金资助课题(桂科攻0816004)
摘 要:目的评价参麦注射液后处理对大鼠心肌缺血再灌注损伤的影响。方法健康雄性SD大鼠32只,10~12周龄,体重240~260g,采用随机数字表法,将其随机分为3组(n=12):假手术组(s组)、缺血再灌注组(I/R组)和参麦注射液后处理组(SPO组)。I/R组和SPO组采用结扎左冠状动脉前降支30min,再灌注120rain的方法制备大鼠心肌缺血再灌注模型;S组只穿线不结扎。于缺血30rain时I/R组静脉注射生理盐水9ml/kg,SPO组静脉注射参麦注射液9ml/kg。再灌注120min时,腹主动脉采集血样,测定血清CK活性和cTnI浓度;然后处死大鼠,取心肌组织,观察病理学结果和细胞凋亡情况,计算心肌细胞凋亡指数,采用免疫组化法检测心肌细胞Bcl-2和Bax的蛋白表达。结果与s组比较,I/R组和SPO组血清CK活性和cTnI浓度升高,I/R组心肌细胞凋亡指数升高,Bcl-2蛋白表达下调,Bax蛋白表达上调,SPO组心肌细胞凋亡指数升高,Bcl-2和Bax的蛋白表达上调(P〈0.01);与I/R组比较,SPO组血清CK活性和cTnJ浓度降低,心肌细胞凋亡指数降低,Bcl-2蛋白表达上调,Bax蛋白表达下调(P〈0.01),病理学损伤减轻。结论参麦注射液后处理可减轻大鼠心肌缺血再灌注损伤,其机制可能与上调Bcl-2蛋白表达,下调Bax蛋白表达,抑制心肌细胞凋亡有关。Objective To investigate the effects of postconditioning with Shemnai-injectio on myocardial ischemia-reperfusion (I/R) injury in rats.Methods Thirty-six healthy male SD rats aged 10-12 weeks weighing 240-260 g were randomly divided into 3 groups (n = 12 each) : sham operation group (group S) ; myocardial I/R group and Shenmai-injectio postconditioning group (group SPO). Myocardial I/R was produced by ligation of the left anterior descending branch of coronary artery for 30 min followed by 120 min reperfusion in groups I/R and SPO. In group SPO Shemnai-injectio 9 ml/kg was injected iv at the end of 30 min ischemia. Blood samples were collected from abdominal aorta at the end of 120 min reperfusion for determination of serum CK activity and cTnI concentration. The animals were then sacrificed. Myocardial specimens were obtained for microscopic examination, detection of apoptosis and determination of myocardial Bcl-2 and Bax protein expression ( by immuno-histochemis- try). Results Myocardial I/R significantly increased serum CK activity, cTnI concentration, apoptotic index (per- centage of apoptotic cells) and Bax protein expression and decreased Bcl-2 protein expression in group I/R as com- pared with group S. Shenmai-injectio postconditioning significantly attenuated I/R-induced above changes and ameliorated histo-pathalogical damage in group SPO as compared with group I/R. Conclusion Shenmai-injectiopostconditioning can reduce myocardial I/R injury by up-regulating Bcl-2 expression and down-regulating Bax expression, leading eventually to reduction in apoptosis.
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