ArticleMolecular and cellular biochemistry2026
Neuroprotective effects of gallic acid against docetaxel-induced peripheral neuropathy: behavioral, molecular, and histopathological evidence.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Hesperidin Attenuates Vincristine-Induced Nephrotoxicity via Nrf2/HO-1 and PI3K/Akt/mTOR Signaling.Journal of biochemical and molecular toxicology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
Indexed as
Identifiers
42573976What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.