Gallic acid protect against spinal cord ischemia-reperfusion injury in rat via activation of Nrf2/HO-1 signaling.

OBJECT

This study explores Gallic acid's (GA) neuroprotective effects against spinal cord ischemia-reperfusion injury (SCII) and its underlying mechanisms.

METHODS

Spinal cord ischemia/reperfusion injury was induced in rats using the modified Zivin's method of clamping the abdominal aorta. The Basso-Beattie-Bresnahan scores, the inclined plane test, hematoxylin and eosin (HE) staining, and Nissl staining were used to measure locomotor activity and histological changes in the injured spinal cords. Proinflammatory factors (TNF-α and IL-1β) were examined using an ELISA kit. Moreover, In vitro oxidative stress model was induced by tBHP used to assess the cell survival rate, reactive oxygen species (ROS) levels, Malondialdehyde (MDA) levels. RT-qPCR and Western blot was used to detect the expression levels of mRNA and proteins.

RESULTS

In vitro, GA inhibited tBHP-induced apoptosis in PC-12 cells, reduced ROS and MDA production, and abolished the expression of pro-apoptotic factors while enhancing the Nrf2/HO-1 signaling pathway. In vivo, GA treatment improved the behavioral and structural aspects of SCII in rats, inhibiting the production of proinflammatory factors, also reduced oxidative stress, and prevented neuronal apoptosis by enhancing the Nrf2/HO-1 signaling pathway.

CONCLUSIONS

GA exhibits neuroprotective effects against SCII, involving antioxidant, anti-inflammatory, and anti-apoptotic activities through Nrf2/HO-1 signaling pathway.