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作 者:宋羽[1,2] 沈祥春[1] 陶玲[1] 张燕[1,3] 肖婷婷[1] 胡函帅[1]
机构地区:[1]贵阳医学院药理学研究室,贵州贵阳550004 [2]南方医科大学第三附属医院药剂科,广东广州510630 [3]新乡医学院第一附属医院,河南新乡453100
出 处:《中国药理学通报》2012年第10期1456-1459,共4页Chinese Pharmacological Bulletin
基 金:国家自然科学基金资助项目(No 81173586;30701024);贵州省高层次人才特助经费(No TZJF-2006-13);贵州省科技攻关项目(No黔科合S字[2011]3010);贵州省国际科技合作项目(No黔科合外G字[2009]700115号)
摘 要:目的观察环维黄杨星D(CVB-D)对去甲肾上腺素(NE)诱导心肌细胞损伤的保护作用及对G蛋白偶联受体激酶-2(GRK-2)表达的影响。方法体外培养新生SD大鼠原代心肌细胞,建立NE诱导的心肌细胞损伤模型,以细胞存活率,培养上清液乳酸脱氢酶的(LDH)活性反映心肌细胞损伤。酶联免疫吸附法(ELISA)测定环磷酸腺苷(cAMP)含量,Western blot分析G蛋白偶联受体激酶-2(GRK-2)蛋白表达。结果 NE能降低细胞存活率,提高培养液LDH活性,降低细胞内cAMP含量,增加GRK-2蛋白表达。CVB-D对NE诱导上述指标异常具有明显的改善作用。Aim To investigate the effects and explore the mechanism of Cyclovirobuxine-D(CVB-D) on expression of GRK-2 in primary culture cardiac myocyte injury induced by norepinephrine(NE).Methods The primary culture cardiac myocyte injury was reproduced by 20 μmol.L-1.The injury was assayed by the cell survivial rate and LDH activity in medium.cAMP content in the cell lysis solution was measured by ELISA,and the GRK-2 protein expression was detected by Western blot.Results NE significantly decreased the cell survivial rate and cAMP contents in cell lysis solution,and increased the LDH activity in medium and GRK-2 protein expression in cell lysis solution.Pretreated with CVB-D,the abnormal was significantly ameliorated in primary culture cardiac myocyte injury induced by NE.Conclusions CVB-D protects against primary culture cardiac myocyte injury induced by NE,and the mechanism may be involved in associating with depression G-protein coupled receptors signaling pathway via increasing the contents of cAMP and down regulating GRK-2 expression.
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