Tempol对过氧化氢致RAW264.7巨噬细胞氧化损伤的保护作用

摘要

Objective:To study the protective effects of tempol on oxidative damage induced by hydrogen peroxide (H2O2) in RAW264.7 cells.Methods:Oxidative damage model of RAW264.7 macrophages was established by H2O2 treatment.RAW264.7 cells were divided into four groups: blank control group, H2O2-injury group (0.2 mmol/L H2O2), Tempol low-dose group (0.2 mmol/L H2O2+0.4 mmol/L tempol) and Tempol high-dose group (0.2 mmol/L H2O2+0.8 mmol/L tempol).The levels of malondialdehyde (MDA), superoxide dismutase (SOD) and lactate dehydrogenase (LDH) were measured in the culture medium of each group.Results:The content of MDA and the activity of LDH were increased in H2O2-injury group compared with blank control group, while the activity of SOD was deceased (all P<0.05).Compared with H2O2-injury group, the content of MDA [(7.27±0.35) nmol/mL and (7.27±0.26) nmol/mL vs.(9.55±0.31) nmol/mL, both P<0.05] and the activity of LDH [(509.36±38.73) U/L and (492.81±40.36) U/L vs.(706.24±48.46) U/L, both P<0.05] in Tempol low-dose group and Tempol high-dose group reduced significantly, while the activity of SOD [(24.84±0.54) U/mL and (24.84±0.28) U/mL vs.(21.16±0.61) U/mL, both P<0.05] increased.There was no significant difference in MDA content, SOD and LDH activity between Tempol low-dose group and Tempol high-dose group, and the effects of tempol were not dose-dependent.Conclusion:Tempol has protective effects on H2O2-induced injury in RAW264.7 cells by regulating cell redox system.%目的:研究4-羟基-2,2,6,6-四甲基哌啶(Tempol)对过氧化氢(H2O2)引起的RAW264.7巨噬细胞氧化损伤的影响.方法:建立H2O2诱导的RAW264.7巨噬细胞氧化损伤模型,分为空白对照组、H2O2损伤组(0.2 mmol/L H2O2)、低剂量Tempol组(0.2 mmol/L H2O2+0.4 mmol/L Tempol)和高剂量Tempol组(0.2 mmol/L H2O2+0.8 mmol/L Tempol),测定每组细胞培养上清液中丙二醛(MDA)含量、超氧化物歧化酶(SOD)和乳酸脱氢酶(LDH)活性.结果:与空白对照组相比,H2O2损伤组培养上清中MDA含量和LDH活性显著升高,SOD活性显著降低(P均< 0.05).与H2O2损伤组相比,低剂量Tempol组与高剂量Tempol组细胞培养上清中MDA的含量[(7.27±0.35) nmol/mL和(7.27±0.26) nmol/mL对(9.55±0.31) nmol/mL, P均<0.05]和LDH的活性[(509.36±38.73) U/L和(492.81±40.36) U/L对(706.24±48.46) U/L,P均<0.05]均显著降低,而SOD的活性[(24.84±0.54) U/mL和(24.84±0.28) U/mL对(21.16±0.61) U/mL, P均<0.05]均显著升高.低剂量Tempol组和高剂量Tempol组MDA含量、SOD和LDH活性无明显差异,Tempol的作用不呈剂量依赖性.结论:Tempol可能通过调节细胞氧化还原系统,对H2O2引起的RAW264.7氧化损伤起到保护作用.