盐酸右美托咪定对H2O2诱导的肺泡巨噬细胞氧化应激的影响

目的：观察n2肾上腺素受体激动剂盐酸右美托咪定是否能够对抗过氧化氢（H2O2）诱导的肺泡巨噬细胞氧化损伤。方法：选择合适浓度H2O2和作用时间建立细胞氧化损伤模型，应用0．01，0．10，1．00umol／L浓度盐酸右美托咪定分别处理24h后，再应用MT比色法检测H2O2诱导的损伤细胞的存活率；用相应试剂盒测定细胞乳酸脱氢酶（1actate dehydrogenase，LDH）和肿瘤坏死因子-α（TNF—α）释放量。结果：50～300Fmol／LH2O2浓度依赖性地引起肺泡巨噬细胞氧化损伤，降低细胞存活率，增加LDH和TNF-a释放。0．01～1．00Fmol／L盐酸右美托咪定可以浓度依赖性地对抗H2O2诱导的细胞氧化损伤，使细胞存活率明显增加，减少LDH和TNF-α释放，这种作用具有剂量依赖性。α2受体拈抗剂育亨宾能够完全拈抗盐酸右美托咪定的这种保护作用，并且育亨宾本身对细胞的氧化损伤没有影响。结论：盐酸右美托咪定能保护肺泡巨噬细胞对抗H2O2诱导的氧化应激损伤，此作用可能通过α2肾上腺素受体发挥作用。

Effect of dexmedetomidine hydrochloride on H2O2-induced oxidative stress in alveolar macrophages

Objective： To evaluate whether dexmedetomidine hydrochloride, an a2-adrenergic receptor agonist, can prevent oxidative damage to alveolar macrophages induced by H2O2. Methods： We used methyl thiazolyl tetrazolium （MqT） colorimetry to test the effect of different concentrations and action time of H202 on the survival rate of alveolar macrophages, and then we chose the appropriate H202 concentration and action time to build NR8383 cell oxidative damage model. After pre-conditioning of 0.01, 0.10, and 1.00 umol/L dexmedetomidine hydrochloride for 24 hours, MTI colorimetry was used to demonstrate the survival rate of NR8383 cells damaged by H202, and the release of lactate dehydrogenase （LDH） and TNF-a by H202-damaged NR8383 cells was detected by corresponding kit.Results： At 50-300 umol/L, H202 caused concentration-dependent oxidative damage in the alveolar macrophages, decreased the cell survival rate, and increased LDH and TNF-a release. At 0.0 I-1.00 tmoI/L dexmedetomidine hydrochloride concentration-dependently protected NR8383 cells from oxidative damage induced by H20 significantly increased the cell survival rate, decreased LDH and TNF-a release, and this effect of dexmedetomidine hydrochloride was dose-dependent. Yohimbine, an a2 - adrenergic receptor antagonist, completely neutralized the protective effect of dexmedetomidine hydrochloride on NR8383 cells without affecting the oxidative damage of NR8383 cells. Conclusion： Dexmedetomidine hydrochloride can prevent alveolar macrophages from oxidative damage induced by H202~ which may play a protective role through a2 - adreneric receptors.