Wogonin inhibits inflammation and apoptosis through STAT3 signal pathway to promote the recovery of spinal cord injury

Spinal cord injury (SCI) is a complex central traumatic disease. STAT3 signal transduction pathway plays an important role in SCI. Wogonin has been reported to exhibit neuroprotection. However, the molecular mechanism of its potential therapeutic effect after SCI remains unclear. In this study, rats were divided into the following groups: Sham; SCI; SCI + wogonin; and SCI + wogonin + colivelin (Colivelin is an effective activator of the STAT3 pathway). Motor function was evaluated by Basso Beattie Bresnahan (BBB) score. Histomorphological changes in the spinal cords were observed by Hematoxylin-eosin (HE) staining and Nissl staining. Western blot, Transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining, and immunofluorescence were used to detect changes in the neuronal inflammation, apoptosis, and STAT3 signal pathway. Western blot and immunofluorescence techniques were also performed to detect the regulatory effect and the underlying mechanism of wogonin on the inflammation and apoptosis of PC12 cells. Experimental results in vivo and in vitro showed that wogonin could promote the recovery of motor function, improve the histopathological morphology, inhibit the activation of the STAT3 signal pathway, and reduce the neuronal inflammation and apoptosis in the rats with SCI. Activation of the STAT3 signal pathway by colivelin reversed the therapeutic effect of wogonin. Therefore, wogonin could inhibit inflammation and apoptosis by inhibiting the STAT3 signal pathway and promote the functional recovery of rats with SCI.

Automated summary

This study reveals that wogonin promotes functional recovery in SCI rats by inhibiting the STAT3 signal pathway and reducing neuronal inflammation and apoptosis.