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作 者:万华印[1] 孔祥平[1] 杨联萍[1] 李茹冰[1] 张宜俊[1]
机构地区:[1]中国人民解放军第四五八医院传染病中心分子生物学科,广东广州510602
出 处:《中国病理生理杂志》2001年第6期481-484,W001,共5页Chinese Journal of Pathophysiology
基 金:"九五"国家重点科技攻关项目! (No.96 - 90 2 -0 1- 0 4)
摘 要:目的 :研究多肽类物质心肌肽素对缺氧 -再给氧损伤心肌细胞的保护作用。方法 :复制培养心肌细胞缺氧 -再给氧损伤模型 ,缺氧 6 0min ,再给氧 30min ,观察心肌肽素对细胞超微结构的影响。以ACAS 5 70进行细胞内游离Ca2 +的定性检测 ;以荧光染料Fura - 2 -AM定量测定细胞内游离Ca2 +浓度 ;以荧光偏振法测定细胞膜脂质流动性。结果 :心肌肽素能使心肌细胞线粒体超微结构的损伤减轻 ;可剂量依赖性地降低 [Ca2 +]i 和提高细胞膜脂质流动性 ;可明显减少Ca2 +伪彩色三维图色彩值。结论 :心肌肽素对缺氧 -再给氧损伤心肌细胞有明显保护作用 ,可能与其降低 [Ca2 +]iAIM: To study the protective effect of cardiomyopeptidin (CMP) attributed to polypeptide on cultured myocardial cells injured by anoxia-reoxygenation.METHODS: The anoxia-reoxygenation injury model were developed, anoxia for 60 min and reoxygenation for 30 min. The effect of CMP on myocardial ultrastructure was observed. [Ca 2+ ] i was estimated with adherent cell analysis and sorting 570(ACAS 570) laser cytometer and measured with fluorescent dye Fura-2-AM, the lipid fluidity of cellular membrane was determined by fluorescence polarization technique. RESULTS: CMP could obviously improve the ultrastructure of myocardial cells and dose-dependently decrease [Ca 2+ ] i and increase the lipid fluidity of cellular membrane, CMP also could markedly reduce the chromaticity value of pseudo-colour graphic model of Ca 2+ . CONCLUSION: Cardiomyopeptidin has an obvious protective effect on cultured myocardial cells injured by anoxia-reoxygenation, this may be related to its effect of decreasing [Ca 2+ ] i and increasing lipid fluidity of cellular membrane. [
分 类 号:R331.31[医药卫生—人体生理学] R972[医药卫生—基础医学]
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