Effects of Dexamethasone on Autophagy and Apoptosis in Acute Spinal Cord Injury

Objectives: To investigate the effects of dexamethasone on autophagy and apoptosis in spinal cord neurons.Methods: We established an in vitro model of spinal cord injury and given different concentrations of dexamethasone at 24 hours after injury. Then we used western blot, MTT, flow cytometry, RT-PCR to detect the level of apoptosis. Western blotting was used to evaluate the expression of LC3. The TEM was used to observe the ultrastructure of the autophagosome. After we give the autophagy inhibitor (3-MA) and autophagy activator (Rapamycin). The autophagy and apoptosis were observed by western blot, flow cytometry, and RT-PCRResults: The results of MTT showed that 10-6 M dexamethasone could increase the activity after cell injury. Meanwhile, flow cytometry, RT-PCR and western blot showed that 10-6 M decreased the apoptosis level. Similarly, autolysosome can be observed after treatment with dexamethasone by electron microscope. At the same time the expression of LC3 protein and beclin-1 gene expression increased. Give autophagy activator (Rapamycin) can increase the level of autophagy, reduce cell apoptosis. In contrast, the autophagy inhibitor (3-MA) inhibits autophagy and increases apoptosis.Conclusion: In conclusion, our observations indicate that dexamethasone inhibited the level of autophagy in the injured nerve cells in a dose-dependent manner. High doses of dexamethasone protected the damaged spinal cord neurons by inhibiting apoptosis, but a protective effect from low hormone concentrations was not obvious.