The mechanistic study of quercetin in the treatment of alcoholic brain injury via the JNK/P38 MAPK signaling pathway.
Level 5 - mechanism / opinion, no new human data
Preclinical laboratory study using cell cultures and animal models with no human subjects.
PubMed 40457147 · doi:10.1007/s10495-025-02125-w
What was done
Researchers evaluated the neuroprotective effects of quercetin against alcohol-induced damage using in vitro and in vivo models. In vitro, BV2 microglia and HT22 neuronal cells were tested for viability (CCK-8), reactive oxygen species (ROS), glutathione, mitochondrial structure via transmission electron microscopy, apoptosis via flow cytometry, and protein expression via Western blot. In vivo, Sprague-Dawley rats were allocated to control, ethanol, or ethanol plus quercetin groups (25, 50, or 100 mg/kg body weight) for 12 weeks, followed by behavioral testing, histological assessment, oxidative stress assays, and protein expression profiling.
What was found
The abstract reports directional changes without numerical values or effect sizes. Quercetin increased superoxide dismutase (SOD) activity, decreased ROS and malondialdehyde (MDA), reduced mitochondrial structural damage, and suppressed apoptosis and inflammatory cytokines (IL-1, IL-6, TNF-α). It also decreased phosphorylated P38 and JNK activation. In rats, quercetin improved spatial cognition, lowered anxiety-like behavior, and attenuated brain oxidative and inflammatory injury.
Why it matters
Alcoholic brain damage lacks highly effective therapeutic options, and this study outlines a mechanistic basis (JNK/P38 MAPK pathway modulation) for quercetin as a candidate neuroprotective agent in preclinical models.
Limits
Findings are entirely preclinical, derived from cell lines and a rodent model, precluding direct clinical translation. The abstract does not provide exact animal sample sizes, specific quantitative effect sizes, confidence intervals, or statistical values. Bioavailability, blood-brain barrier penetration in humans, and potential adverse effects of chronic high-dose quercetin were not assessed.
Cited by
- supports Alcohol consumption depletes glutathione levels in the brain.