LAUSR

Introduction: Crush injuries occur from acute traumatic nerve compression resulting in different degrees of neural damage leading to permanent functional deficits. Recently, we have shown that administration of Fraction B (FB) derived from catfish epidermal secretions accelerates healing of damaged nerve in a sciatic nerve crush injury, as it ameliorates the neurobehavioral deficits and enhances axonal regeneration, as well as protects spinal neurons and increases astrocytic activity and decreasing GAP-43 expression. The present study aimed to investigate the role of FB treatment on the apoptotic pathway in the neuroregeneration of the sciatic nerve crush injury. Methods: Male Wistar rats were randomly assigned into five groups: (I) SHAM, (II) CRUSH, (III) CRUSH + (1.5 mg/kg) FB, (IV) CRUSH + (3 mg/kg) FB, and (V) CRUSH + (4.5 mg/kg) FB. Rats underwent sciatic nerve crush surgery, followed by treatment with FB administered intraperitoneally (IP) daily for two weeks and then sacrificed at the end of the fourth week. Results: FB improved the recovery of neurobehavioral functions with a concomitant increase in axonal regeneration and neuroprotective effects on spinal cord neurons following crush injury. Further, FB enhanced Schwann cells (SCs) proliferation with a significant increase in myelin basic protein expression. FB-treated animals demonstrated higher numbers of neurons in the spinal cord, possibly through ameliorating oxidative DNA damage and alleviating the mitochondrial-dependent apoptotic pathway by inhibiting the release of cytochrome c and the activation of caspase-3 in the spinal cord neurons. Conclusion: FB alleviates the neurodegenerative changes in the lumbar spinal cord neurons and recovers the decrease in the neuronal count through its anti-apoptotic and DNA antioxidative properties.