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BioMed Research International
Volume 2017, Article ID 2017493, 12 pages
https://doi.org/10.1155/2017/2017493
Research Article

Electrospun Nanofibers Loaded with Quercetin Promote the Recovery of Focal Entrapment Neuropathy in a Rat Model of Streptozotocin-Induced Diabetes

1Department of Physiology and Graduate School (Neuroscience Program), Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand
2Integrative Complementary and Alternative Medicine Research and Development Center, Khon Kaen University, Khon Kaen 40002, Thailand
3Department of Physiology, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand

Correspondence should be addressed to Jintanaporn Wattanathorn; moc.oohay@wnropanatnij

Received 17 October 2016; Accepted 29 December 2016; Published 30 January 2017

Academic Editor: Stelvio M. Bandiera

Copyright © 2017 Chonlathip Thipkaew et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

In this study, quercetin-loaded zein-based nanofibers were developed using electrospinning technique. The therapeutic effect of these quercetin-loaded nanofibers on neuropathy in streptozotocin- (STZ-) induced diabetes in rats was assessed. Diabetic condition was induced in male Wistar rats by STZ, after which a crush injury of the right sciatic nerve was performed to induce mononeuropathy. Functional recovery was assessed using walking track analysis, measurements of foot withdrawal reflex, nerve conduction velocity, and morphological analysis. The oxidative stress status and the ratio of phosphorylated extracellular recognition kinase (pERK)/extracellular recognition kinase (ERK) expression in the nerve lesion were also assessed in order to elucidate the potential mechanisms involved. Results showed that quercetin-loaded zein-based nanofibers slightly enhanced functional recovery from neuropathy in STZ-diabetic rats. The potential mechanism might partially involve improvements in oxidative stress status and the ratio of pERK/ERK expression in the nerve lesion.