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研究的主要目的旨在探讨卡托普利和西卡普鲁斯特对培养新生乳鼠心肌细胞缺氧缺糖时膜流动性改变的保护作用。为了探讨其它与膜相关的改变,我们同时观察了培养细胞缺氧时脂质过氧化水平及乳酸脱氢酶(LDH)的释放情况。采用荧光分光光度计测定稳态荧光各向异性(r_s)的改变来监测膜流动性,脂质过氧化水平通过测定硫代巴比妥酸反应物(简称 TBARS)含量来评估。实验表明卡托普利(180μmol/L)、西卡普鲁斯特(30 nmol/L)和消炎痛(1μmol/L)对正常新生乳鼠心肌细胞的 r_s 值、TBARS 水平及 LDH 活性均无影响,卡托普利和西卡普鲁斯特均能显著阻止缺氧缺糖所致心肌细胞 r_s 值、TBARS 含量和 LDH 释放的增加,且均有剂量依赖性。消炎痛能取消卡托普利对 TBARS 产生及 LDH 释放的作用,但是仍保留膜流动性的保护作用。这些结果说明卡托普利和西卡普鲁斯特具有保护心肌细胞缺氧损伤时膜流动性和脂质过氧化的作用。卡托普利的保护作用可能是通过促进前列环素的合成和/或释放介导的。
The main purpose of this study was to investigate the protective effect of captopril and cisapride on the changes of membrane fluidity in cultured neonatal rat cardiomyocytes subjected to hypoxia-glucose deprivation. To explore other membrane-associated changes, we also observed the level of lipid peroxidation and lactate dehydrogenase (LDH) release in cultured cells during hypoxia. The membrane fluidity was monitored by measuring the steady-state fluorescence anisotropy (r_s) using a fluorescence spectrophotometer. Lipid peroxidation levels were assessed by measuring the thiobarbituric acid reactant (TBARS) content. The results showed that r_s value, TBARS level and LDH activity of captopril (180μmol / L), Xiupulute (30nmol / L) and indomethacin (1μmol / L) Both captopril and western plutonium significantly prevented r_s, TBARS and LDH release induced by oxygen and glucose deprivation in a dose-dependent manner. Indomethacin abolished the effect of captopril on TBARS production and LDH release, but retained the protective effect of membrane fluidity. These results suggest that captopril and cisapride have the effect of protecting membrane fluidity and lipid peroxidation during cardiomyocyte hypoxia injury. Captopril’s protective effect may be mediated through the promotion of prostacyclin synthesis and / or release.