右美托咪定对抗化学性低氧引起的PC12细胞损伤

目的探讨α2肾上腺素受体激动剂右美托咪定能否保护PC12细胞对抗化学性低氧引起的损伤。方法应用化学性低氧模拟剂氯化钴(CoCl2)处理PC12细胞以建立化学性缺氧损伤模型。应用CCK-8比色法检测细胞存活率;Ho-chest 33258核染色法观察细胞凋亡的形态学和数量的改变;双氯荧光素(DCFH-DA)染色荧光显微镜检测细胞内的活性氧(ROS)水平;罗丹明123(Rh123)染色荧光显微镜检测线粒体膜电位(MMP)。结果在浓度为100～600μmol.L-1的范围内,右美托咪定浓度依赖性地对抗CoCl2引起的细胞毒性,使细胞存活率明显增加。400μmol.L-1右美托咪定能抑制CoCl2的致凋亡作用,使凋亡细胞数量减少。右美托咪定也能抑制CoCl2引起的ROS过度生成及MMP降低的作用。结论右美托咪定能保护PC12细胞对抗CoCl2诱导的损伤,此作用可能与其抑制ROS过度生成及保护MMP有关。

Dexmedetomidine protects neurons against chemical hypoxia-induced injury

Aim To explore whether alpha(α)-2-adrenoreceptor agonist dexmedetomidine protects PC12 cells against chemical hypoxia-induced injury.Meth-ods PC12 cells were treated with cobalt chloride(CoCl 2)to set up a chemical hypoxia-induced injury model.Cell viability was measured by cell counter kit(CCK-8).Morphological changes and number of apoptotic cells were detected by Hochest33258 staining,Intracellular level of reactive oxygen species(ROS)was tested by DCFH-DA staining and photofluorography.Mitochondrial membrane potential(MMP)was observed by rhodamine 123(Rh123)staining and photofluorography.Results At concentrations from 100 to 600μmol·L-1,dexmedetomidine dose-dependently inhibited CoCl2-induced cytotoxicity,increasing cell viability.Dexmedetomidine at 400μmol·L-1attenuated CoCl2-induced apoptotic effect,decreasing the number of apoptotic cells.Dexmedetomidine could also reduce overproduction of ROS and MMP loss induced by CoCl2.Conclusion Dexmedetomidine can protect PC12 cells against CoCl2-induced injury,which may be associated with its inhibitory effect on overproduction of ROS and preservation of MMP.