丙泊酚预处理对大鼠心肌细胞缺血再灌注损伤的保护作用

Protective Effect of Propofol Preconditioning (pretreatment)on Ischemia/Reperfusion (Anoxia/Reoxygenation) Injury of Myocardial Cells in Rats

目的 探讨丙泊酚对缺氧 /复氧心肌细胞损伤的保护作用及可能机制。方法 将原代培养的乳鼠心室肌细胞分为正常对照与丙泊酚不同浓度处理组 ,分别以 0、 12 5、 2 5、 5 0、 10 0 μmol/L丙泊酚预处理 2 0min后 ,予以缺氧3h复氧 1h。结果 与对照组相比 ,单纯缺氧 /复氧 (0 μmol/L组 )细胞活力与超氧化物歧化酶 (SOD)活性显著下降 ,乳酸脱氢酶 (LDH)、肌酸激酶 (CK)、丙二醛 (MDA)水平显著升高 (P <0 0 1)。丙泊酚预处理以剂量依赖性减轻细胞活力下降及LDH、CK水平上升 ,并拮抗MDA水平上升及SOD活性下降的作用 (P <0 0 1或 0 0 5 ) ,2 5μmol/L组保护作用达峰值 (P <0 0 1)。结论 丙泊酚以剂量依赖性保护缺氧 /复氧心肌细胞损伤 ,2 5 μmol/L该作用达峰值。

Objective To investigate the protective effect of propofol on anoxia/reoxygenation injury in cultured myocardial cells and possible mechanism. Methods Primary cultured myocardial cells of rats were randomly allocated to 6 groups: control group (A) not subject to any treatment; propofol preconditioning groups (0, 12 5, 25, 50, 100 μmol/L preconditioning for 20 min followed by 3 h anoxia and 1 h reoxygenation). Results Compared with control group, the levels of lactate dehydrogenase (LDH) and creatine kinase (CK), and the content of cellular malondiadehyde (MDA) were significantly increased, while the cell viability and the activity of superoxide dismutase (SOD) were markedly decreased in single anoxia/reoxgeneration group (0 μmol/L group) ( P <0 01). Propofol preconditioning could significantly attenuate the increased LDH, CK level and the decreased cell viability in a dose dependent manner ( P <0 01 or 0 05), and antagonize the elevated MDA level and the reduced SOD activity ( P <0 01 or 0 05). 25 μ mol/L propofol showed the greatest protective effect ( P <0 01). Conclusion Propofol could protect the myocardial cells from anoxia/reoxygenation injury in a dose dependent manner and 25 μmol/L propofol showed the greatest protective effects. The mechanism may be related to the ability of propofol against the oxidant injury.