Effect and Molecular Mechanism of Wnt/β-Catenin Signaling Pathway on Apoptosis after Spinal Cord Injury

Secondary injury plays a more important role in the development of spinal cord injury (SCI), mainly due to apoptosis, inflammatory response, oxidative stress and other causes, especially neuronal cell apoptosis inhibits the nerve function recovery after SCI. In recent years, the study of wnt signaling after SCI has attracted more attention. Wnt signal pathway is divided into three kinds of signal pathway: the classic signal path (wnt/β-catenin); non-classical signal path (wnt/JNK) and Wnt-Ca2+ signal path. Previous studies have shown that cellapoptosis activity is activated after inhibition of the wnt/β-catenin signaling pathway in other systemic diseases of the body, while there is no clear description on correlation between wnt/β-catenin signaling pathway and apoptosis after SCI. In our previous study, we found that wnt/β-catenin signaling pathway was negatively correlated with neuronal apoptosis at different time points after SCI. We will continue to demonstrate the effect of inhibition of activation or activation of wnt/β-catenin signaling pathway on neuronal cell apoptosis and the effect on neurological function in vivo and in vitro experiments after SCI. This is the first observation of the relationship between wnt/β-catenin signaling pathway and neuronal apoptosis after SCI. The role of wnt/β-catenin signaling pathway in the recovery of neurological function after SCI and its molecular mechanism may provide a new therapeutic target and program for treating SCI, and provide a strong theoretical basis and experimental basis for the basic study of SCI.