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目的研究内质网通路在氯胺酮(Ketamine)致SH-SY5Y细胞凋亡中的作用。方法采用0.0、12.5、25.0、50.0和100.0μg/ml的氯胺酮处理SH-SY5Y细胞48 h时,采用MTT比色法检测细胞的生长率;荧光探针检测细胞内活性氧;流式细胞仪检测细胞凋亡和胞内钙离子浓度;Western blot检测CHOP蛋白的表达量。结果与空白对照组相比,所有氯胺酮处理组细胞活力均显著降低,活性氧显著升高(P<0.05或P<0.01);胞内钙离子浓度和CHOP蛋白表达量,除12.5μg/ml氯胺酮处理组外均显著升高(P<0.05或P<0.01)。与未处理对照组相比,细胞凋亡率25.0、50.0和100.0μg/ml氯胺酮处理组显著升高(P<0.01)。结论一定浓度氯胺酮可通过内质网通路引起人神经母细胞瘤SH-SY5Y细胞凋亡的发生。
Objective To investigate the role of endoplasmic reticulum (ER) pathway in apoptosis of SH-SY5Y cells induced by Ketamine. Methods SH-SY5Y cells were treated with ketamine at concentrations of 0.0, 12.5, 25.0, 50.0 and 100.0 μg / ml for 48 h. MTT assay was used to detect the growth of SH-SY5Y cells. Fluorescence probe was used to detect the intracellular ROS. Flow cytometry Apoptosis and intracellular calcium concentration were detected by Western blot. Results Compared with the blank control group, the viability of all Ketamine treated groups was significantly decreased and the reactive oxygen species was significantly increased (P <0.05 or P <0.01). The intracellular calcium concentration and the expression of CHOP protein, except 12.5μg / ml ketamine The treatment group were significantly higher (P <0.05 or P <0.01). Compared with the untreated control group, the apoptotic rates of 25.0, 50.0 and 100.0 μg / ml ketamine groups were significantly increased (P <0.01). Conclusions Ketamine can induce the apoptosis of human neuroblastoma SH-SY5Y cells through the endoplasmic reticulum pathway.