3,4-methylenedioxymethamphetamine induces reactive oxygen species-mediated autophagy and thioredoxin-interactive protein/nucleotide-binding domain, leucine-rich containing family, pyrin domain-containing-3 inflammasome a
Lee SY., Chiu SW., Li IH., Tsai WC., Li CH.
Laboratory Study, published in J Dent Sci (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- J Dent Sci (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 40654447
- PMCID
- PMC12254870
- DOI
- 10.1016/j.jds.2025.04.025
Abstract (original English)
Background/purpose 3,4-methylenedioxymethamphetamine (MDMA) is a synthetic substituted amphetamine. Research primarily focuses on its neurotoxicity and psychological effects, while studies examining its impact on mesenchymal stem cells (MSCs) and dental pulp stem cells (DPSCs) are relatively limited. This study investigated the cytotoxicity and molecular mechanisms of MDMA in DPSCs. Materials and methods Cell viability, apoptosis, autophagy, immunophenotype, reactive oxygen species (ROS), and the related signaling pathways were analyzed using a cell counting kit, Western blot, flow cytometry, and 2',7'-dichlorofluorescein diacetate (DCFH-DA) dye after treating DPSCs with indicated concentrations of MDMA. Results MDMA significantly decreased cell viability and increased cleaved poly adenosine diphosphate-ribose polymerase (PARP), cleaved caspase-8, cleaved caspase-3, and Bcl-2-associated X protein (Bax), while reducing B-cell lymphoma 2 (Bcl-2). Annexin V and 7-aminoactinomycin D (7-AAD) flow cytometry showed that these cells underwent early apoptosis without altering MSCs' immunophenotypic properties. MDMA also induced ROS accumulation and nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome activation. Autophagy activation was observed with adenosine monophosphate-activated protein kinase (AMPK) activation, protein kinase B
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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