ArticleMolecular biology reports2026
Neuroprotective role of stigmasterol through restoration of ubiquitin-proteasome gene expression in an MPTP-induced rodent model of Parkinson's disease.
Article in Molecular biology reports, 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundParkinson’s disease (PD) is second most common neurodegenerative disorder characterized by gradual loss of dopaminergic neurons in the substantia nigra. Its pathophysiology reflects interlinked processes of oxidative stress, inflammation, and altered gene expressions of ubiquitin-proteasome pathway. The current therapy, L-DOPA (Sinemet) provides only symptomatic relief without modifying disease progression. This study aimed to evaluate stigmasterol, a bioactive phytocompound having antioxidant and anti-inflammatory properties and blood brain barrier permeability, as a potential candidate for modifying disease progression in PD.
methodsPD was induced in mice using neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Animals were randomly assigned to five groups: healthy control (HC), MPTP only (PC), MPTP + Sinemet (SC), MPTP + stigmasterol therapeutic (StigTx), and stigmasterol preventive (StigPre). Oxidative stress markers, inflammatory mediators (IL-1β, IL-6, TNF-α, CRP), hepatic and renal markers were evaluated. Dopaminergic neuronal survival was examined by tyrosine hydroxylase immunostaining, and PD-related gene expression (PRKN, PINK1, UCHL1, LRRK2) was analysed.
resultsMPTP exposure caused marked motor decline, strong oxidative stress and inflammation. Sinemet partially improved motor functions and antioxidant status but showed limited effects on lipid peroxidation and induced mild hepatic stress. In contrast, stigmasterol reduced inflammation, enhanced antioxidant defences, and improved motor ability without inducing organ toxicity. Preventive use showed more promising results by preserving dopaminergic neurons and modulated PD related gene expression.
conclusionStigmasterol improves motor dysfunction and provides significant neuroprotection, highlighting its potential as a multitarget therapeutic candidate capable of modifying disease related molecular pathways.
Indexed as
Identifiers
42047872What 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.