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机构地区:[1]第二军医大学药学院药理学教研室 [2]第二军医大学东方肝胆外科医院药剂科
出 处:《第二军医大学学报》1998年第1期45-47,共3页Academic Journal of Second Military Medical University
摘 要:目的:研究维生素E(VE)、普罗布考(PRB)对溶血卵磷脂(LPC)引起的脑微血管内皮细胞(BCMEC)损伤的保护作用和脑微血管平滑肌细胞(BCMSMC)增殖的抑制作用。方法:以乳酸脱氢酶(LDH)释放及结晶紫染色法分别测定BCMEC损伤和BCMSMC的增殖。结果:VE5~50μmol/L时显著抑制LPC50nmol/L引起的BCMEC释放LDH,释放率下降至(36.8±1.0)%~(16.2±2.9)%;显著抑制LPC10nmol/L引起的BCMSMC增殖,抑制率为(37.6±7.0)%~(61.3±0.6)%。PRB5~50μmol/L时显著抑制LPC50nmol/L引起的BCMEC释放LDH,释放率下降至(34.2±3.3)%~(19.1±2.4)%;显著抑制LPC10nmol/L引起的BCMSMC增殖,抑制率为(40.9±2.4)%~(47.0±3.7)%。结论:VE和PRB对LPC引起的BCMEC损伤有保护作用,对BCMSMC增殖有抑制作用。Objective: To investigate the protective effects of vitamin E(VE) and probucol (PRB) on the injury and proliferation of cerebral microvascular cells. Methods: The injury of bovine cerebral microvascular endothelial cells (BCMEC) was determined by the lactic dehydrogenase (LDH) release and the proliferation of bovine cerebral microvascular smooth muscle cells (BCMSMC) with crystal violet staining. Results: VE of 5 to 50 μmol/L inhibited BCMEC from releasing LDH induced by LPC of 50 nmol/L, releasing rate declined to (36.8±1.0) % to (16.2±2.9)%, and inhibited BCMSMC proliferating induced by LPC of 10 nmol/L, with inhibitory rate of (37.6±7.0)% to (61.3±0.6)%. PRB of 5 to 50 μmol/L inhibited BCMEC from releasing LDH induced by LPC of 50 nmol/L, releasing rate declined to (34.2±3.3)% to (19.1±2.4)%, and inhibited BCMSMC from proliferating induced by LPC of 10 nmol/L, with inhibitory proliferation rate of (40.9±2.4) % to (47.0±3.7) %. Conclusion: VE and PRB have protective effects on the injury of BCMEC and the proliferation of BCMSMC induced by LPC.
关 键 词:维生素E 普罗布考 内皮细胞 LPC 动脉粥样硬化
分 类 号:R543.505[医药卫生—心血管疾病]
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