Abstract
Background
The secondary injury plays a vital role in the development of Spinal cord injury (SCI), which characterized by the occurrence of oxidative stress, neuronal apoptosis, and inflammatory response. Notoginsenoside R1 (NGR1) has been involved in the modulation of anti-oxidative stress and anti-inflammatory response. However, its roles in SCI-induced injury are still unknown.
Methods
Sprague-Dawley rats were subjected to SCI through a weight-drop method. the therapeutic effect of NGR1 and its underlying mechanism after SCI were explored by using behavioral, biochemical, and immunohistochemical techniques.
Results
The administration of NGR1 after SCI enhanced the neurological function, mitigated tissue damage, and motor neuron loss than those in SCI + vehicle group. Meanwhile, significantly increased expression of Nrf2 protein and HO-1 protein was found in the SCI + NGR1 group compared with those in the SCI + vehicle group. In addition, the inhibitory effects of oxidative stress, apoptotic neuron ratio, and neuronal inflammation in the SCI + NGR1 group can be partially reversed when the Nrf2/HO-1 signaling pathway was inhibited by ML385.
Conclusions
The administration of NGR1 after SCI can attenuate oxidative stress, neuronal apoptosis, and inflammation by activating the Nrf2/HO-1 signaling pathway after SCI, thereby improving neurological function.
Treatment With 2-BFI Attenuated Spinal Cord Injury by Inhibiting Oxidative Stress and Neuronal Apoptosis via the Nrf2 Signaling Pathway
