Neuroprotective effects of gallic acid against docetaxel-induced peripheral neuropathy: behavioral, molecular, and histopathological evidence.

Authors

Özge Kandemir, Hasan Şimşek, Tuğba Çelik Samancı, Fatih Mehmet Kandemir

Published in

Molecular and cellular biochemistry. Aug 10, 2026. Epub Aug 10, 2026.

Abstract

This study focuses on the potential neuroprotective effects of gallic acid (GA) against docetaxel (DOC)-induced peripheral neuropathy, which arises particularly through oxidative stress and limits the clinical use of this effective anti-mitotic chemotherapy agent. Twenty-eight Wistar rats were randomly assigned to four groups (n = 7): Control (saline), Gallic acid (GA, 200 mg/kg/day, oral), Docetaxel (DOC, 30 mg/kg, single dose i.p.), and Docetaxel + Gallic acid (DOC + GA). Peripheral neuropathy due to DOC and the potential protective effects of GA were evaluated using behavioral tests, oxidative stress and antioxidant parameters, RT-PCR, histopathological and GFAP/BDNF immunohistochemical analyses. DOC administration significantly impaired motor functions. GA treatment administered concurrently with DOC significantly improved these behavioral impairments (p < 0.001). Additionally, DOC increased MDA levels and decreased antioxidant defenses (GSH, SOD, CAT, GPx), whereas GA reversed these changes. GA also significantly suppressed DOC-induced inflammation (NF-κB, TNF-α, nNOS; p < 0.001), apoptosis (caspase-3, Bax, Bcl-2; p < 0.001), autophagy (Beclin-1, LC3A; p < 0.001), and endoplasmic reticulum stress (PERK, ATF6; p < 0.001). Morphological and immunohistochemical analyses demonstrated that GA partially repaired DOC-induced sciatic nerve damage, characterized by decreased GFAP immunoreactivity and improved BDNF expression. This study provides a comprehensive evaluation of the multitarget effects of GA on oxidative stress-related and stress-associated molecular pathways in a DOC-induced peripheral neuropathy model, offering preliminary insight into its potential as a supportive therapeutic approach.

PMID:
42573976
Bibliographic data and abstract were imported from PubMed on 10 Aug 2026.

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