右美托咪定对抗化学性低氧引起的PC12细胞损伤

Dexmedetomidine protects neurons against chemical hypoxia-induced injury

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。

Abstract： Aim To explore whether alpha （e） -2-ad- renoreceptor agonist dexmedetomidine protects PC12（CoC12） 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, In- tracellular level of reactive oxygen species （ROS） was tested by DCFH-DA staining and photofluorography. Mitochondrial membrane potential （MMP） was ob- served by rhodamine 123 （Rh123） staining and photo- fluorography. Results At concentrations from 100 to 600 μmol· L-1, dexmedetomidine dose-dependently inhibited CoC12-induced cytotoxicity, increasing cellcells against chemical hypoxia-induced injury. Meth- ods PC 1 2 cells were treated with cobalt chlorideviability. Dexmedetomidine at 400 μmol · L-1 attenua- ted CoC12-induced apoptotic effect, decreasing the number of apoptotic cells. Dexmedetomidine could also reduce overproduction of ROS and MMP loss induced by CoC12. Conclusion Dexmedetomidine can protect PC12 cells against CoC12-induced injury, which may be associated with its inhibitory effect on overproduction of ROS and preservation of MMP.