ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Neuroprotective effects of hydroxytyrosol against monosodium glutamate-induced hippocampal and cerebellar injury in rats.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Monosodium glutamate (MSG) is a widely used food additive associated with neurotoxicity through excitotoxicity, oxidative stress, neuroinflammation, and apoptosis. The present study investigated the neuroprotective effects of hydroxytyrosol (HT), a naturally occurring phenolic compound with antioxidant and anti-inflammatory properties, against MSG-induced brain and cerebellar injury in rats. Thirty-two male Wistar albino rats were randomly assigned to four groups (Control, MSG, HT, and MSG + HT). MSG (2 g/kg) and HT (10 mg/kg) were administered intraperitoneally for 21 days. Oxidative stress markers, inflammatory cytokines, myelin basic protein (MBP), histopathological alterations, and immunohistochemical markers of glial activation and apoptosis were evaluated. MSG administration significantly increased malondialdehyde (MDA), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) levels while decreasing glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and MBP levels in both brain and cerebellar tissues. Histopathological examination revealed marked neuronal degeneration, whereas immunohistochemical analyses demonstrated increased GFAP, S100β, and Bax expression together with reduced Bcl-2 immunoreactivity. HT treatment markedly attenuated these biochemical, histopathological, and immunohistochemical alterations by restoring antioxidant defenses, suppressing inflammatory responses, preserving MBP expression, reducing glial activation, and improving the Bax/Bcl-2 balance. These findings demonstrate that HT exerts neuroprotective effects against MSG-induced brain and cerebellar injury through coordinated antioxidant, anti-inflammatory, myelin-preserving, and anti-apoptotic mechanisms. The integrated evaluation of biochemical, histopathological, and immunohistochemical alterations highlights HT's potential as a promising candidate for preventing oxidative and inflammatory neurotoxicity.
Indexed as
Identifiers
42907674What 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.