右美托咪定抑制化学性低氧引起的PC12细胞炎症反应

Dexmedetomidine inhibits inflammation induced by chemical hypoxia in PC12 cells

目的探讨右美托咪定(dexmedetomidine,DEX)能否抑制化学性缺氧引起的PC12细胞炎症反应。方法用氯化钴(CoCl2)处理PC12细胞,建立化学性低氧诱导的细胞损伤实验模型;ELISA法检测细胞培养液中白介素6(IL-6)、白介素1β(IL-1β)和肿瘤坏死因子α(TNF-ɑ)的水平;以CCK-8法检测细胞存活率。结果 CoCl2处理PC12细胞能产生明显的炎症反应,导致IL-6、IL-1β和TNF-ɑ释放增多;IL-6、IL-1β和TNF-ɑ的中和抗体能抑制CoCl2导致的细胞存活率下降。DEX和活性氧(ROS)抑制剂N-乙酰半胱胺酸(NAC)不但能抑制CoCl2引起的上述炎症因子的释放,而且使PC12细胞存活率升高。结论 DEX可通过抑制炎症反应和抗氧化作用对抗化学性缺氧引起的PC12细胞毒性。

Aim To investigate whether dexmedetomi- dine（DEX） protects PC12 cells against inflammation reaction induced by chemical hypoxia. Methods PC12 cells were exposed to 600 μmol · L-1 cobalt chloride to establish a model of chemical hypoxia-in- duced injury. The levels of interleukin 1 β （ IL-1β）, in- terleukin 6 （IL-6） and tumor necrosis factor a （ TNF- a） were detected by ELISA. Cell viability was detec- ted by CCK-8. Results Exposure of PC12 cells to 600 μmol · L-1 CoC12 induced inflammatory reaction, leading to an increase in the secretion of IL-1 β, IL-6 and TNF-a. Neutralizing antibodies for the anti- IL- 1β, or anti-IL-6, or anti- TNF-ctstatistically alleviated CoC12-induced cytotoxicity in PC12 cells. DEX （0. 1μmol · L-1 ） and 500 μmol · L-1 NAC （ a reactive ox- ygen species scavenger） not only inhibited the in- creased inflammatory factors mentioned above, but also increased the cell viability of PC12 cells. Conclusion DEX protects PC12 cells against chemical hypoxia- induced cytoxicity through inhibiting inflammatory re- action and antioxidation.