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作 者:谭洪玲[1] 马增春[1] 肖成荣[1] 王宇光[1] 梁乾德[1] 洪倩[1] 陆倍倍[1] 刘明[1] 高月[1]
机构地区:[1]军事医学科学院放射与辐射医学研究所,北京100850
出 处:《解放军药学学报》2010年第3期194-197,共4页Pharmaceutical Journal of Chinese People's Liberation Army
基 金:军队科技攻关项目;No.08g144
摘 要:目的观察红景天苷抗心肌缺氧/复氧损伤的保护作用,探讨红景天苷抗心肌缺氧可能的信号通路。方法原代培养的心肌细胞加入不同浓度的红景天苷缺氧24h,噻唑蓝法测定细胞增殖;原代培养的心肌细胞分为5组:正常对照组;缺氧/复氧组;缺氧/复氧加红景天苷100μg/ml组;缺氧/复氧加红景天苷100μg/ml再加细胞外调节激酶抑制剂20μg组;缺氧/复氧加细胞外调节激酶抑制剂20μg组。加药后先孵育60min,再缺氧培养4h,随后常氧培养2h。全自动生化分析仪测定心肌酶(乳酸脱氢酶、肌酸肌酶、谷草转氨酶)含量,Westernblot法检测细胞外信号调节激酶蛋白表达。结果红景天苷增加了缺氧/复氧损伤心肌细胞的活力,降低了心肌细胞乳酸脱氢酶和肌酸激酶的渗漏,使磷酸化细胞外信号调节激酶蛋白表达水平明显降低。结论红景天苷对缺氧诱导的心肌细胞损伤有保护作用,此作用可能通过细胞外信号调节激酶信号通路发挥作用。Objective To investigate the effect of salidroside on neonatal rat cardiocytes damaged by hypoxia /reoxygenation and to study signal pathways invovled in the mechanism of salidroside.Methods Some primarily cultured cardiomyocytes of neonatal rats were pretreated with different concentrations of salidroside,and cultrued in hypoxia for 24 h.The cell viability was measured by 3-[4,5-dimethyithiazol]-2,5-diphenyl tetrazolium bromide assay.Some were pretreated with different concentrations of salidroside,and cultrued in hypoxia for 4 h and in reoxygenation for 1 h.The activities of lactate dehydrogenase,glutamic oxalacetic transamine and creatin kinase were measured by colorimetric method.The expression of extracellular signal regulated kinase was determined by Western blot method.Results Compared with hypoxia group,pretreatment with different concentrations of salidroside significantly attenuated hypoxia-induced cell viability loss and dramatically decreased the activities of the lactate dehydrogenase and creatin kinase.The phosphorylation of extracellular signal regulated kinase was decreased by salidroside.Conclusion Salidroside can protect rat cardiomyocytes from the injury induced by hypoxia/reoxygenation,and extracellular signal regulated kinase plays a key role in the mechanism of salidroside.
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