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Original Research Article | OPEN ACCESS

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

Jie Huang, Xinghua Tan

Department of Pharmacy, Shaoxing Stomatological Hospital, Shaoxing, China;

For correspondence:-  Xinghua Tan   Email: tth0203@163.com   Tel:+8613034265755

Accepted: 29 January 2023        Published: 27 February 2023

Citation: Huang J, Tan X. Protective effect of epalrestat on peripheral nerves in rats with diabetic peripheral neuropathy via NF-κB pathway. Trop J Pharm Res 2023; 22(2):239-244 doi: 10.4314/tjpr.v22i2.3

© 2023 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

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.

Keywords: Diabetic peripheral neuropathy, Epalrestat, NF-κB, Apoptosis

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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