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.
出处
《交通医学》
2007年第1期17-19,共3页
Medical Journal of Communications
