ArticleNeurochemical research2025
Sinomenine Modifies Parkinson's Disease Through Nrf2 Activation.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- Hyperoside Exerts Therapeutic Effects on Parkinson's Disease by Mitigating Oxidative Stress through Activation of Nrf2/HO-1 Pathway.Chinese journal of integrative medicine · 2026Article
- Neuroprotective effect of sinomenine on parkinson's disease through NLRP3/Caspase-1/GSDMD pathway-mediated pyroptosis inhibition.Metabolic brain disease · 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
14 authors.
Funding
Abstract
backgroundDisease-modifying treatments for Parkinson's disease (PD) are urgently needed, with the Nrf2/ARE pathway a promising target. This study aims to explore the effects of sinomenine on PD and Nrf2/ARE activation.
methods6-OHDA-treated Parkinsonian SH-SY5Y cells and rats were used. Apoptosis and cell viability were measured using flow cytometry and CCK-8 assays. Nrf2 and its downstream proteins were assessed by Western blotting, while ROS levels were detected with fluorescent dyes. Nrf2 silencing via shRNA evaluated sinomenine's dependence on Nrf2 activation. In vivo, behavioral changes, tyrosine hydroxylase (TH) levels and malondialdehyde (MDA) levels were measured. Microglial inflammation was analyzed by measuring TNF-α and IL-1β expression and cytoskeleton analysis. Nrf2 nuclear translocation was verified by Western blotting and molecular docking was performed.
resultsSinomenine reduced apoptosis and ROS, improved cell viability, upregulated Nrf2 and antioxidant enzyme expression. The protective effects against apoptosis were abolished by Nrf2 silencing. In PD animals, sinomenine improved motor deficits, enhanced Nrf2, GCLC, GCLM, NQO1, and HO-1 expression, decreased MDA levels, increased TH levels in the striatum and maintained count of dopaminergic neurons in substantia nigra. Additionally, it suppressed TNF-α and IL-1β levels in brain tissue and blood, preserving normal microglial morphology and reducing neuroinflammation. Sinomenine promoted Nrf2 nuclear translocation and showed high Keap1 affinity in docking.
conclusionsSinomenine activates the Nrf2/ARE pathway, mitigating oxidative stress and inflammation in PD models, possibly through Keap1 binding and Nrf2 nuclear translocation. These findings suggest sinomenine may serve as a potential disease-modifying therapy for Parkinson's disease, pending further clinical validation.
Indexed as
Identifiers
40965719What 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.