Objective: To observe the effects of dexamethasone (DEX) on rat PC12 chromaffin tumor cells and glucose uptake.
Methods: PC12 cells in vitro were randomized into normal control group, 10 and 100 μmol/L DEX treated groups. MTT assay was used to determined the cell viability to evaluate the optimal concentration of DEX. Cell apoptosis was measured by DAPI fluorescence staining, mitochondrial membrane permeability transition pore (mPTP), activities of caspase-3 and caspase-9. Glucose oxidase and peroxidase (GOD-POD) assay was performed to detect the glucose consumption. Expression of glucose transporter 3 (GLUT-3) was detected by Western blotting.
Results: Compared with the control group, (10, 100) μmol/L DEX significantly decreased cell vitality, caused apoptosis, and reduced the glucose uptake and GLUT-3 protein level (P<0.05).
Conclusion: DEX can induce the apoptosis of PC12 cells, the mechanism of which may be related to inhibited GLUT-3 protein expression and glucose uptake.