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作 者:赵素玲[1] 王洪新[1] 周振华[1] 喻晓春[2] 鲁美丽[1] 宋莹[1] 张晶[1]
机构地区:[1]辽宁医学院分子生物学与新药开发重点实验室,辽宁锦州121001 [2]中国中医科学院实验中心,北京100700
出 处:《中国药理学通报》2011年第12期1682-1686,共5页Chinese Pharmacological Bulletin
基 金:国家自然科学基金资助项目(No 30973898/C190702);辽宁省高等学校优秀人才支持计划(No 2008RC33)
摘 要:目的探讨黄芪多糖(APS)对异丙肾上腺素(isoprot-erenol,Iso)诱导的乳鼠心肌细胞肥大的保护作用及机制。方法以原代培养乳鼠心肌细胞为模型,应用Iso 10μmol.L-1诱导心肌细胞肥大,观察不同浓度的黄芪多糖及L型钙通道阻滞剂维拉帕米(Verapamil,VER)对心肌肥厚的影响。用Lowry法测心肌细胞蛋白含量;消化分离法及计算机图像分析系统测细胞体积;RT-PCR法检测心肌细胞ANP的mR-NA表达;以Fluo-3/AM为荧光探针,采用激光共聚焦显微镜观察细胞内[Ca2+]i的变化。结果 APS和VER均能够有效抑制Iso诱导的心肌细胞肥大,表现为蛋白质含量降低,体积减小,ANP mRNA表达降低和细胞内钙离子浓度降低,且APS的作用呈一定的剂量依赖性。结论黄芪多糖对Iso诱导乳大鼠心肌细胞肥大有保护作用,其机制可能与降低[Ca2+]i有关。Aim To investigate the protective effects and mechanism of isoproterenol-induced neonatal rat cardiomyocyte hypertrophy by Astragalus polysaccharides(APS).Methods The primary cultures of neonatal rat ventricular myocytes were used as models,the hypertrophic cardiac myotecytes were induced by isoproterenol 10 μmol·L-1,and the effect of different concentrations of APS and the L-type calcium channel blocker Verapamil on cardiac hypertrophy was observed.Total protein content was assayed by Lowry method;the size of cardiomyocytes was measured by computer photograph analysis system;the expression of ANP mRNA was determined by RT-PCR;intracellular [ca2+] i changes were measured by confocal laser microscopy and by cell-loading Fluo-3/AM.Results APS and Verapamil were able to inhibit the Iso-induced cardiac hypertrophy,expressed as the protein content and volume decreased,the expression of ANP mRNA decreased and the intracellular calcium ion concentration reduced.APS had a dose-dependent inhibitory effect.Conclusions APS has a protective effect on ISO-induced cardiac hypertrophy.The mechanism may be related to the inhibition of [ca2+] i.
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