Protective effect of epalrestat on peripheral nerves in rats with diabetic peripheral neuropathy via NF κB pathway

Abstract

Purpose: To study the protective effect of epalrestat on peripheral nerves in rats with diabetic peripheral neuropathy (DPN).
 Methods: A total of 36 Sprague-Dawley rats were randomly divided into normal, model, and epalrestat groups, each containing 12 rats. The morphology of the neurons was assessed using hematoxylin-eosin (H&E) staining. The expressions of B-cell lymphoma-2 (Bcl-2), and Bcl-2 associated X protein (Bax) were determined via immunohistochemistry. The relative protein expressions of NF-κB and Caspase3 were determined via Western blotting, and apoptosis was determined using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay.
 Results: The morphology of the neurons was clear and intact in the normal group, disordered and destroyed in the model group, and was improved in the epalrestat group. The other two groups had a significantly higher positive expression of Bax and a significantly lower positive expression of Bcl-2 than the normal group (p < 0.05), while the epalrestat group had a significantly lower positive expression of Bax, and a significantly higher positive expression of Bcl-2 than the model group (p < 0.05). Furthermore, the protein expressions of NF-κB and Caspase3 were increased in other groups compared with normal group (p < 0.05), while they declined in epalrestat group compared with model group (p < 0.05). The apoptosis rate was significantly lower in epalrestat group than in model group (p < 0.05).
 Conclusion: Epalrestat inhibits neuronal apoptosis by suppressing the NF-κB signaling pathway, thereby exerting a neuroprotective effect in DPN rats. Further studies would be required to validate the molecular mechanism.