Evidence map›Paper›PMID 42262723›Full record

ArticleJournal of biochemical and molecular toxicology2026

Cannabidiol Protects Against 1-Methyl-4-Phenylpyridinium and Manganese-Induced Neurotoxicity via Nod-Like Receptor Protein 3 Inflammasome Suppression.

Göksun Demirel, Anıl Yirün, Deniz Arca Çakir, Hüseyin Özkan, Berfu Şura Güneş, Selen Selvi, Yeter Erol Öztürk, Pınar Erkekoğlu

Abstract read
In one paragraph

Article in Journal of biochemical and molecular toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Göksun DemirelDepartment of Pharmaceutical Toxicology, Çukurova University Faculty of Pharmacy, Adana, Turkey.ORCID https://orcid.org/0000-0002-2994-5505
Anıl YirünDepartment of Pharmaceutical Toxicology, Çukurova University Faculty of Pharmacy, Adana, Turkey.
Deniz Arca ÇakirDepartment of Pharmaceutical Toxicology, Hacettepe University Faculty of Pharmacy, Ankara, Turkey.
Hüseyin ÖzkanDepartment of Genetics, Faculty of Veterinary Medicine, Hatay Mustafa Kemal University, Hatay, Turkey.ORCID https://orcid.org/0000-0001-5753-8985
Berfu Şura GüneşDepartment of Pharmaceutical Toxicology, Çukurova University Faculty of Pharmacy, Adana, Turkey.
Selen SelviDepartment of Pharmaceutical Toxicology, Çukurova University Faculty of Pharmacy, Adana, Turkey.
Yeter Erol ÖztürkDepartment of Chemistry, Council of Forensic Medicine, Ankara, Turkey.
Pınar ErkekoğluDepartment of Pharmaceutical Toxicology, Hacettepe University Faculty of Pharmacy, Ankara, Turkey.ORCID https://orcid.org/0000-0003-4713-7672

Funding

Health Institutes of Turkey (TÜSEB) 43052
6 · The paper itself

Abstract

Parkinson's disease (PD) is a neurodegenerative disorder characterized by dopaminergic neurodegeneration, alpha-synuclein (α-Syn) accumulation, and neuroinflammation. The NOD-Like Receptor (NLR) family pyrin domain containing 3 NLRP3 inflammasome has recently been identified as a central mediator of PD-associated inflammatory responses. Cannabidiol (CBD), a non-psychoactive phytocannabinoid, exhibits anti-inflammatory and neuroprotective properties; however, its effects on NLRP3 inflammasome in PD remain insufficiently understood. This study investigated the neuroprotective effects of CBD-rich oil against 1-methyl-4-phenylpyridinium (MPP+) and manganese-induced neurotoxicity in SH-SY5Y cells. Cells were exposed to these substances with or without CBD co-treatment, and cell viability, α-Syn, dopamine, inflammatory markers [C reactive protein (CRP) and interleukin 18 (IL-18)], and NLRP3 expressions were evaluated. MPP+ and manganese exposures significantly decreased cell viability and dopamine levels while increasing α-Syn accumulation and inflammatory markers. Manganese induced an approximately twofold upregulation in NLRP3 mRNA and 1.5-fold increase in protein expression. CBD co-treatment preserved dopamine levels, attenuated α-Syn accumulation, reduced IL-18 and CRP concentrations, and attenuated NLRP3 expression. These findings demonstrate that CBD-rich oil exerts neuroprotective effects in a PD cellular model by attenuating α-Syn accumulation, preserving dopamine homeostasis, which is associated with reduced NLRP3 expression and potential modulation of inflammasome-related signaling, supporting further investigation of CBD as a potential therapeutic strategy for PD.

Indexed as

1-Methyl-4-phenylpyridiniumCannabidiolInflammasomesManganeseNeuroprotective AgentsNLR Family, Pyrin Domain-Containing 3 Proteinalpha-SynucleinCell Line, TumorCell SurvivalHumans1-Methyl-4-phenylpyridiniumalpha-SynucleinCannabidiolInflammasomesManganeseNeuroprotective AgentsNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humancannabidiolmanganeseMPP+neuroinflammationNLRP3 inflammasomeParkinson's diseaseα‐synuclein

Identifiers

PMID42262723
PMCPMC13249025

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.