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出 处:《交通医学》2007年第1期17-19,共3页Medical Journal of Communications
摘 要:目的:研究丙泊酚对缺氧/复氧培养大鼠心肌细胞LDH漏出及HSP70表达的影响。方法:建立SD大鼠心肌细胞原代培养及缺氧/复氧模型。将原代培养大鼠心肌细胞分为6组,I组为对照组;II组为缺氧/复氧对照组;III组为在缺氧前开始加入脂肪乳;IV、V和VI组在缺氧前开始加入丙泊酚25μmol/L、50μmol/L和100μmol/L。在复氧4h时用免疫组化法和图像平均灰度法测定HSP70的表达,在复氧3h时用生化比色法测培养基中LDH活力。结果:3种浓度丙泊酚均能减少心肌细胞LDH漏出(P<0.05)。II组与I组比较HSP70表达明显增加,VI组与II组比较HSP70表达明显被抑制,平均灰度值差异有统计学意义(P<0.05)。结论:3种浓度的丙泊酚能防治心肌细胞缺氧/复氧损伤。Objective:To observe the effect of propofol on HSP70 expression in cultured cardiac myocytes of neonatal rats and the concentration of lactate dehydrogenase (LDH) in culture medium during reoxygenation.nethods:Original cultured cardiomyocytes of SD rats and hypoxia-reoxygenation injuried immature cardiomyocyte were established.The 36 cases of cultured cardiac myocytes were divided into 6 groups:Group Ⅰ as control;Group Ⅱ as hypoxia-reoxygenation(hypoxia 4 hours-reoxygenation 4 hours)control;Compared to Group Ⅱ,Groups Ⅲ,Ⅳ,Ⅴ and Ⅵ were treated with intelipid or propofol (251μmol/L, 50μmol/L and 100μmol/L)since 10min before hypoxia respectively.Immunohistochemistry and mean gray were used to estimate the effect of propofol on the expression of HSP70 in cultured rat cardiomyocytes in 4 cases of each group 4h after reoxygenation.Release of lactate dehydrogenase of the cardiomyocytes in the other 2 cases of each group were investigated and determined as injury index of eardiomyocytes.Result:Release of lactate dehydrogenase was inhibited by propofol in 3 kinds of density,and the expression of HSP70 of the cardiomyocytes was significantly inhibited by propofol in 100μmol/L(P〈0.05).Conclusion:Hypoxia-reoxygenation injury of the cardiomyocytes was released,and then the expression of HSP70 during reoxygenation was inhibited.
分 类 号:R542.2[医药卫生—心血管疾病]
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