摘要
目的探讨丙泊酚预处理对大鼠嗜铬细胞瘤株(PC12)细胞高温损伤的影响及其可能的机制。方法体外培养PC12细胞,分为4组:正常对照组(C组),常规(37℃)培养;高温损伤组(H组),将细胞置于46℃培养箱中2 h,随后恢复常规培养;丙泊酚预处理+高温损伤Ⅰ组(P1+H组)和丙泊酚预处理+高温损伤Ⅱ组(P2+H组)将细胞分别于高温损伤前置于37℃培养箱中以含丙泊酚终浓度25,50μmol.L-1培养液作用1 h,余同H组处理。处理完毕后四甲基偶氮唑盐(MTT)法测定细胞活力,乳酸脱氢酶(LDH)法检测细胞损伤,测定细胞内超氧化物歧化酶(SOD)活性和丙二醛(MDA)水平反映抗氧化活性。结果与H组比较,P1+H组和P2+H组MTT值升高(P<0.01),LDH释放量减少(P<0.01),同时细胞内SOD活性增高,MDA生成量明显减少。P1+H组和P2+H组之间比较,各指标差异无显著性(P>0.05)。结论丙泊酚预处理对PC12细胞高温损伤有保护作用,这一作用可能与其抗氧化作用有关。
Objective To explore the effect of propofol preconditioning on lethal heat-induced rat pheochromoeytoma （ PC12 ） cells injury and the possible mechanism. Methods PC 12 cells were divided into 4 groups： control group, cells were untreated; lethal heat （H） group, cells were exposed to lethal heat （46℃ for 2 h） ; （P1 ＋ H） group and （P2 ＋ H） group in which propofol was added to the culture medium （the final concentrations of propofol were 25 μmol ·L^-1 and 50 μmol· L^-1 respectively ） 1 h before exposed to lethal heat. MTT assay and LDH leakage were performed to study the eytotoxieity, superoxide dimutase （SOD） activity and malondialdehyde（MDA） formation were measured to reflect the activity of antioxidase. Results Compared with H group, elevation of MTT cell activity （ P 〈 0, 01 ）, and reduction of LDH leakage （ P 〈 0.01 ） in （ P1 ＋ H） group and （P2 ＋ H） group were displayed, the activity of SOD was markedly decreased（P 〈 0.01 ） , and the content of cellular MDA was significantly increased（ P 〈 0.01 ）. But there were no significant difference between （P1 ＋ H） group and （P2 ＋ H） group（P 〉0.05）. Conclusion Propofol preconditioning produces protective effect against lethal heat-induced PC12 cells injury. The mechanism may be related to the ability of propofol against the oxidant injury.
出处
《医药导报》
CAS
2007年第9期996-998,共3页
Herald of Medicine
