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作 者:罗萍[1] 杜松[1] 段红艳[1] 李海霞[2] 韩沐芮[3]
机构地区:[1]河南省人民医院心内科,郑州450003 [2]河南省人民医院检验科,郑州450003 [3]中国药科大学药学院,江苏南京211198
出 处:《医药论坛杂志》2011年第19期8-11,共4页Journal of Medical Forum
基 金:河南省科技厅基础与前沿项目;编号:112300410049
摘 要:目的探讨普罗布考对过氧化氢(H2O2)诱导的心肌细胞凋亡的影响,探讨其可能的机制。方法培养的新生鼠心肌细胞随机分组并给予0.2mmol.L-1H2O2或0.2mmol.L-1 H2O2及不同浓度的普罗布考(100μmol.L-1、10μmol.L-1和1μmol.L-1)。采用琼脂糖凝聚电泳检测细胞凋亡;逆转录聚合酶链式反应(RT-PCR)法检测细胞Bcl-2 mRNA及Bax mRNA表达;黄嘌呤氧化酶法测定细胞内超氧化物歧化酶(SOD)活性,硫代巴比妥酸法检测细胞内丙二醛(MDA)含量。结果普罗布考明显抑制H2O2诱导的心肌细胞凋亡,降低心肌细胞BaxmRNA表达,升高Bcl-2mRNA表达。经不同浓度普罗布考干预后,心肌细胞SOD活性显著升高,MDA含量显著降低。以上这些效应均呈剂量依赖性。结论普罗布考抑制H2O2诱导的心肌细胞凋亡,其作用机制与改善心肌细胞氧化应激水平有关。Objective To observe the effect of probucol on cardiomyocyte hydrogen peroxide( n2 02 ) and to explore its possible mechanisms. Methods apoptosis induced by Cultured neonatal rat cardiomyocytes were divided randomly to receive 0. 2mmol. L - 1 H202 or 0, 2mmol. L - 1 H2O2 plus different concentrations of probucol ( 1μmol. L - 1,10μmol. L - 1,100μmol. L - 1 ). Apoptosis cells were assessed by flow agarose gel eletrophoresis. The mRNA expression of Bcl -2 and Bax in cardio- myocytes were determined by reverse transcriptase -polymerase chain reaction (RT- PCR). The su- peroxide dismutase(SOD) activity and malondialdehyde (MDA) content in cells were tested by xan- thine oxidase method and color reaction of thiobarbituric acid method, respectively. Results Probucol significantly decreased H202 induced cardiomyocyte apoptosis as well as the increased mRNA expression of Bcl - 2 and the decreased mRNA expression of Bax. After pretreated with proubcol, SOD activity was increased and MDA content was declined significantly. All these effects were in a dose inde- pendent manner. Conclusions Probucol inhibited H20/ induced cardiomyocytes apoptosis partly by reducing the oxidative stress level.
分 类 号:R332[医药卫生—人体生理学]
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