检索规则说明:AND代表“并且”;OR代表“或者”;NOT代表“不包含”;(注意必须大写,运算符两边需空一格)
检 索 范 例 :范例一: (K=图书馆学 OR K=情报学) AND A=范并思 范例二:J=计算机应用与软件 AND (U=C++ OR U=Basic) NOT M=Visual
机构地区:[1]辽宁省心脑血管药物基础研究重点实验室辽宁医学院药物研究所,辽宁省锦州市121001
出 处:《中国动脉硬化杂志》2010年第11期845-848,共4页Chinese Journal of Arteriosclerosis
基 金:国家自然科学基金(30973898);辽宁省教育厅优秀人才基金(2008RC33)
摘 要:目的探讨黄芪甲苷对高糖诱导的心肌细胞肥大的保护作用。方法利用体外培养模型,以25mmol/L高糖诱导心肌肥大。新生大乳鼠心肌细胞分为正常对照组、高糖组、高糖+16μmol/L黄芪甲苷组、高糖+32μmol/L黄芪甲苷组和高糖+64μmol/L黄芪甲苷组,用Lowry法检测心肌细胞蛋白含量;消化分离法及计算机图像分析系统检测心肌细胞体积;MTT法检测细胞存活率;采用Till阳离子测定系统,以Fura-2/AM为荧光探针,观察心肌细胞[Ca2+]i的瞬间变化。结果与正常对照组相比,高糖使心肌细胞蛋白质含量增加35.7%,体积增大81.3%,[Ca2+]i瞬变增加62.5%%,心肌细胞存活率降低36.1%。加入16μmol/L黄芪甲苷后,与高糖组相比,心肌细胞蛋白质的含量和细胞体积分别降低20.3%和10.6%,[Ca2+]i瞬间变化降低8.0%,心肌细胞的存活率增加20.0%。结论黄芪甲苷对高糖诱导的乳大鼠心肌细胞肥大具有保护作用。Aim To investigate the protective effects of astragaloside Ⅳ on high glucose induced cardiomyocyte hypertrophy in neonatal rats. Methods Myocardial cells of neonatal rats were cultured in vitro,the hypertrophic myocytes were induced by 25 mmol/L high glucose(HG).Cultured neonatal rats' cardiomyocytes were divided into normal group,HG group,HG+16 μmol/L astragaloside Ⅳ,HG+32 μmol/L astragaloside Ⅳ,HG+64 μmol/L astragaloside Ⅳ,48 h later,total protein content was assayed by Lowry method.The cardiomyocyte volume was measured by computer photogragh analysis system.The cardiomyocyte viability was analysed by MTT assay.i transient was measured by Till image system and by cell-loading Fura-2/AM. Results Compared with normal control group,HG increased the total protein content,cardiomyocoytes size,i transient by 35.7%,81.3%,62.5% and decreased the cardiomyocyte viability by 36.1%.Compared with HG group,astragaloside Ⅳ 16 μmol/L reduced the total protein content,cardiomyocoytes size,i transient by 20.3%,10.6%,8.0% and cardiomyocyte viability was inceased by 20.0%.There was dose-dependent relationship. Conclusion astragaloside Ⅳ could protect cardiomyocyte hypertrophy in glucose-induced rats.
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在链接到云南高校图书馆文献保障联盟下载...
云南高校图书馆联盟文献共享服务平台 版权所有©
您的IP:216.73.216.229