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

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... lished 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.