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目的观察地塞米松(DEX)诱导PC12大鼠嗜铬瘤细胞凋亡及对葡萄糖摄取的影响。方法体外培养的PC12细胞随机分为正常对照组、10μmol/L DEX组、100μmol/L DEX组。MTT法测细胞存活率,DAPI荧光染色、线粒体膜通透性转换孔(mPTP)、capase-3、caspase-9活性测定细胞凋亡。葡萄糖氧化酶-过氧化物酶法测葡萄糖的摄取率,Western blot法检测葡萄糖转运子3(GLUT-3)的表达。结果与正常对照组比较,DEX作用PC12细胞48 h,DEX组细胞活力下降、引起细胞凋亡;DEX组葡萄糖的摄取下降,GLUT-3蛋白水平下降(P<0.05)。结论 DEX可以诱导PC12细胞凋亡,其机制可能与DEX引起细胞GLUT-3蛋白表达水平下降引起葡萄糖摄取下降有关。
Objective To observe the apoptosis of pheochromocytoma cells induced by dexamethasone (DEX) in PC12 rats and its effect on glucose uptake. Methods PC12 cells cultured in vitro were randomly divided into normal control group, 10μmol / L DEX group and 100μmol / L DEX group. Cell viability was measured by MTT assay, apoptosis was detected by DAPI staining, mitochondrial membrane permeability transition pore (mPTP), capase-3 and caspase-9 activity. Glucose uptake rate was measured by glucose oxidase-peroxidase method, and glucose transporter 3 (GLUT-3) expression was detected by Western blot. Results Compared with normal control group, DEX treatment induced PC12 cells for 48 h, and cell viability decreased in DEX group, leading to apoptosis; DEX group decreased glucose uptake and GLUT-3 protein decreased (P <0.05). Conclusion DEX can induce the apoptosis of PC12 cells. The mechanism may be related to the decrease of GLUT-3 protein expression induced by DEX and the decrease of glucose uptake.