This study aims to determine the influence of neurotrophin-3 (NT-3) plasmids on neuronal apoptosis and Ca(2+)-ATP enzyme levels in injured muscles. We also investigated the mechanism underlying the role of NT-3 in delaying muscle atrophy following a peripheral nerve injury. Sixty adult Wistar rats were used to generate the peripheral nerve injury models. The rats were randomly assigned to the saline and NT-3 groups. Related indicators, such as caspase-3 protein expression, skeletal muscle cell apoptosis, and Ca(2+)-ATP enzyme expression were quantified. The expression levels of caspase-3 and the histone-muscle cell apoptosis rate in the NT-3 group decreased at different post-operative times following peripheral nerve injury, whereas NT-3 expression and the sarcoplasmic reticulum Ca(2+)-ATP enzyme levels increased. Statistically significant differences were observed in the NT-3 group as compared to the saline group (P < 0.05). NT-3 mitigated muscle atrophy following peripheral nerve damage by inhibiting caspase-3 gene expression and increasing Ca(2+)-ATP enzymatic activity, ultimately reducing muscle apoptosis.
Keywords: Caspase-3; Neurotrophin 3; mechanism; muscle cell apoptosis; peripheral nerve injury.