Spinal cord injury (SCI) as a serious neurological disease remains the great challenge for clinical therapy. Existing studies have confirmed that selenium (Se) supplementation could effectively decrease the risk of neurological diseases, but the mechanism is still unclear. Herein, a mouse SCI model was established, and the potential of selenomethionine (SeMet) against SCI was explored. Behavioral studies showed that SeMet administration in vivo effectively improved the motor symptoms of SCI mice. Mechanism investigation indicated that SeMet administration in vivo significantly blocked the decrease of neurons and Nissl bodies in SCI mice by inhibiting neural apoptosis. SeMet in vivo also dramatically attenuated oxidative damage of SCI mice by regulating the Nrf‐2/Keap‐1 pathway. Further studies revealed that SeMet in vivo significantly alleviated microglia activation and neuroinflammation in SCI mice, as demonstrated by the improved Iba‐1 and inflammatory factors expression, respectively. Moreover, SeMet in vivo apparently inhibited SCI‐induced cell ferroptosis of SCI mice by balancing ferroptosis‐related protein expression. Taken together, the results indicated that oxidative damage–mediated apoptosis and ferroptosis both contributed to the protective potential of SeMet against SCI, which validated the possibility that selenium‐containing agents could be promising drugs for SCI therapy.
Li et al. (Thu,) studied this question.