盐酸右美托咪定对H2O2诱导的库普弗细胞氧化应激和炎性反应的影响

目的：观察α2肾上腺能受体激动剂盐酸右美托咪定能否抑制过氧化氢(H2O2)诱导的库普弗细胞(Kupffer cells，KCs)氧化应激和炎性反应。方法：分离和培养KCs，分别用盐酸右美托咪定或育亨宾处理24 h后，以H2O2作用30 min建立细胞氧化损伤模型，应用MTT比色法检测H2O2诱导的损伤细胞的存活率；用相应的试剂盒测定各组细胞上清液中乳酸脱氢酶(lactate dehydrogenase，LDH)、丙二醛(malonaldehyde，MDA)和肿瘤坏死因子-α (TNF-α)释放量。结果：盐酸右美托咪定显著抑制H2O2诱导的KCs的损伤，提高细胞的存活率，抑制上清液中LDH，MDA，TNF-α释放，这种作用可以被α2受体拮抗剂育亨宾完全拮抗，而育亨宾本身对细胞的氧化损伤和炎性反应没有影响。结论：盐酸右美托咪定可以减轻H2O2诱导的KCs的氧化应激和炎性反应，其可能是通过α2肾上腺能受体发挥作用。

Effect of dexmedetomidine hydrochloride on H2O2-induced oxidative stress and inflammatory response in Kupffer cells

Objective: To evaluate whether dexmedetomidine hydrochloride, an α2-adrenergic receptor agonist, can prevent H2O2-induced oxidative stress and inflammatory response in Kupffer cells. Methods: H2O2-induced oxidative damage model of Kupffer cell was established. Kupffer cells were pre-conditioned by dexmedetomidine hydrochloride or Yohimbine for 24 h. MTT colorimetry was used to demonstrate the survival rate of Kupffer cells. The levels of lactate dehydrogenase (LDH), malonaldehyde (MDA) and TNF-α in the culture medium were assessed by corresponding kits. Results: Dexmedetomidine hydrochloride protected Kupffer cells from H2O2-induced oxidative damage, showing an increase in the cell survival rate while a decrease in LDH, MDA and TNF-α release in the culture supernatant. Yohimbine, an α2-adrenergic receptor antagonist, completely neutralized the protective effect of Dexmedetomidine hydrochloride on Kupffer cells. Yohimbine itself had no effect on H2O2-induced oxidative damage and inflammatory response. Conclusion: Dexmedetomidine hydrochloride can prevent H2O2-induced oxidative stress and inflammatory response in Kupffer cells through activation of α2-adrenergic receptors.