Original Article Neuroprotective effects of diosgenin in rats with experimental spinal cord injury via promotion of autophagy

Bo Zhang, Yanwen Chen, Binhui Yang, Fenglong Jiang, Jinlong Zhao, Zhen Ouyang
2017 Int J Clin Exp Med   unpublished
Spinal cord injury (SCI) is a devastating disorder in the central nervous system with neurologi-cal deficits and loss of motor function. The aim of the present study was to evaluate the neuroprotective effects of diosgenin (DSG), a natural extract which exerts anti-inflammatory effects on many diseases, in a rat model of SCI. Methods: Forty Sprague-Dawley rats were randomized into four groups (Sham group, Vehicle group, DSG (100 mg/ kg) group and DSG (200 mg/kg) group). SCI rat models were
more » ... at models were established based on the Allen's method. DSG was orally administrated (100, 200 mg/kg b.w., respectively) after induction of SCI for consecutive 21 days. Neurological function recovery was evaluated using the Basso, Beattie, Bresnahan (BBB) open-field locomotor rating scale and Rivlin's inclined plane test. Seven days after SCI, the production of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6), was assessed using enzyme-linked immu-nosorbent assay (ELISA) kits to examine the inflammatory responses in perilesional tissues. Western blot analysis was performed to investigate the expression of apoptosis-associated proteins (Bcl-2, Bax, cleaved caspase-3) and autophagy associated proteins (Beclin 1 and light chain 3-II (LC3-II)). Spinal neurons were cultured to investigate the anti-inflammation effect of DSG in vitro. Results: We observed that administration of DSG significantly alleviated SCI-induced neurological deficits. Compared with Vehicle group, treatment with DSG following SCI markedly reduced the production of TNF-α, IL-1β and IL-6. Moreover, compared with Vehicle group, administration of DSG also evidently attenuated SCI-induced apoptosis, and enhanced SCI-induced autophagy. Besides, administration of DSG significantly reduced the levels of TNF-α, IL-1β and IL-6 in LPS-treated spinal cord neurons, and this reduction was suppressed by CQ treatment. Conclusion: Taken together, the results clearly showed that DSG attenuates SCI-induced secondary injury through inhibiting the inflammatory response, repressing apoptosis, and promoting autophagy in perilesional tissues.