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目的 研究不同浓度异丙酚对原代培养新生Wister大鼠海马神经细胞缺氧复氧损伤的影响及其相关机制。方法 在96孔无菌培养板上原代培养10d的海马神经细胞随机分为6组:对照组(Con组)为异丙酚溶剂,即含2‰DMSO的生理盐水;异丙酚1μmol／L浓度组(Pro1组);异丙酚10μmol／L浓度组(Pro10组);异丙酚50μmol／L浓度组(Pro50组);异丙酚100μmol／L浓度组(Pro100组)及异丙酚200 μmol／L浓度组(Pro200组)。各组细胞在给药后均接受3 h缺氧和24 h复氧,分别以单溶液细胞增殖测试法和非放射测定法测定细胞存活能力及乳酸脱氢酶(LDH)漏出率。48孔无菌培养板原代培养10 d的海马神经细胞随机分为上述6组,采取同样给药及缺氧复氧模式,用硫代巴比妥酸比色测定法和黄嘌呤氧化酶化学发光测定法分别测定丙二醛(MDA)浓度和超氧化物歧化酶(SOD)活性。结果 异丙酚各组细胞存活能力高于Con组(P<0.05),而LDH漏出率低于Con组(P<0.05),但异丙酚各组之间差异无显著性。Pro1组和Pro10组MDA浓度低于Con组(P<0.05),随异丙酚浓度进一步增高MDA产生有增多趋势而与Con组相当。Pro1组SOD活性高于Con组(P<0.05),随异丙酚浓度递增各组活性降低,尤其在Pro100和Pro200μmol／L两组。结论 异丙酚在临床相关浓度(1 μmol／L)水平能显著减轻缺氧复氧对
Objective To investigate the effects of different concentrations of propofol on hypoxia-reoxygenation injury in primary cultured neonatal Wistar rats and its related mechanisms. Methods Hippocampal neurons cultured for 10 days on 96-well sterile plates were randomly divided into 6 groups: control group (Con group) was propofol solvent, that is, saline containing 2 ‰ DMSO; propofol 1 μmol / L Group (Pro1 group), propofol 10μmol / L group (Pro10 group), propofol 50μmol / L group (Pro50 group), propofol 100μmol / L group / L concentration group (Pro200 group). The cells in each group were exposed to 3 hours of hypoxia and 24 hours of reoxygenation after administration. Cell viability and lactate dehydrogenase (LDH) leakage rate were determined by single cell proliferation assay and non-radioactive assay respectively. 48-well sterile culture plate primary cultured 10 days hippocampal nerve cells were randomly divided into the above 6 groups, taking the same administration and hypoxia-reoxygenation mode, thiobarbituric acid colorimetric assay and xanthine oxidase chemistry Luminescence assay was used to determine the concentration of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD). Results The cell viability of propofol groups was higher than that of Con group (P <0.05), while the leakage rate of LDH was lower than that of Con group (P <0.05). However, no significant difference was found between propofol groups. The concentrations of MDA in Pro1 group and Pro10 group were lower than those in Con group (P <0.05). With the further increase of propofol concentration, the production of MDA increased with the increase of Pro group and Con group. The activity of SOD in Pro1 group was higher than that in Con group (P <0.05), and decreased with increasing propofol concentrations, especially in Pro100 and Pro200μmol / L groups. Conclusion Propofol at a clinically relevant concentration (1 μmol / L) significantly attenuates hypoxia-reoxygenation