Abstract
The impact of peripheral nerve damage on a patient's quality of life is severe. The most frequent peripheral nerve crush damage is a sciatic nerve injury. Previous research has shown that glibenclamide (GB) has neuroprotective properties in a variety of oxidative stress-related disorders, including Alzheimer and Parkinson. The goal of this study was to see how GB affected nerve regeneration and improved function of the sciatic nerve in a rat model following a crush injury. We evaluated motor function, sensory recovery, gene expression, and histomorphometry following damage at different time points. Additionally, we assessed atrophy in the gastrocnemius muscle using histology and mass ratio analyses. Our results suggest that 2-, 4-, 6-, and 8-weeks following glibenclamide therapy, promotes the recovery of motor and sensory function in the injured site. Following glibenclamid injection, the mRNA levels of neurotrophic factors (NGF and BDNF) are raised. According to histomorphometry assessment, glibenclamide injection also increased the number of myelinated fibers while decreasing their thickness. These results showed that glibenclamide therapy by decreasing the proinflammatory and oxidant factors may enhance the nerve regeneration. It is clear that more research is needed to confirm these findings.
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