ArticleMedical science monitor : international medical journal of experimental and clinical research2019
Methamphetamine Induces Intestinal Inflammatory Injury via Nod-Like Receptor 3 Protein (NLRP3) Inflammasome Overexpression In Vitro and In Vivo.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 24 citations in OpenAlex.
- Roles of gut and oral microbiota in methamphetamine-induced multi-organ toxicity.Cell biology and toxicology · 2026Review
- Body talk: Correlates of gut-immune dysregulation phenotypes in people living with HIV who use methamphetamine.Brain, behavior, & immunity - health · 2026Article
- The effect of neuroimmune signalling on drug addiction.Frontiers in pharmacology · 2026Review
- The impact of endurance training on reducing inflammatory markers in the cardiac tissue of methamphetamine-exposed rats.PloS one · 2026Article
- Article
- Design and Evaluation of a Broadly Multivalent Adhesins-Based Multi-Epitope Fusion Antigen Vaccine Against EnterotoxigenicVaccines · 2025Article
- Intestinal barrier damage caused by addictive substance use disorder.European journal of medical research · 2025Review
- Mechanism analysis and intervention strategies of the inflammatory microenvironment in traumatic spinal cord injury.Frontiers in immunology · 2025Review
- Therapeutic targeting of neuroinflammation in methamphetamine use disorder.Future medicinal chemistry · 2025Review
- Can Methamphetamine-Induced Cardiotoxicity be Ameliorated by Aerobic Training and Nutrition Bio-shield Superfood Supplementation in Rats After Withdrawal?Cardiovascular toxicology · 2024Article
- The Common Denominators of Parkinson's Disease Pathogenesis and Methamphetamine Abuse.Current neuropharmacology · 2024Review
- Microglia NLRP3 Inflammasome and Neuroimmune Signaling in Substance Use Disorders.Biomolecules · 2023Review
- Methamphetamine Induces Systemic Inflammation and Anxiety: The Role of the Gut-Immune-Brain Axis.International journal of molecular sciences · 2022Article
- Dopamine D1 receptors mediate methamphetamine-induced dopaminergic damage: involvement of autophagy regulation via the AMPK/FOXO3A pathway.Psychopharmacology · 2022Article
- Methamphetamine Use: A Narrative Review of Adverse Effects and Related Toxicities.Health psychology research · 2022Article
- Related Effects of Methamphetamine on the Intestinal BarrierFrontiers in medicine · 2022Review
- The Role of Melatonin on NLRP3 Inflammasome Activation in Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- Interactions of neuroimmune signaling and glutamate plasticity in addiction.Journal of neuroinflammation · 2021Review
- The Association of Altered Gut Microbiota and Intestinal Mucosal Barrier Integrity in Mice With Heroin Dependence.Frontiers in nutrition · 2021Article
- NLRP3 Inflammasome: A Promising Therapeutic Target for Drug-Induced Toxicity.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Methamphetamine (METH), a confirmed neurotoxic drug, has also reportedly caused several intestinal inflammatory injury cases. The NLRP3 (Nod-like receptor 3 protein) inflammasome can induce several inflammatory injuries by activating IL-1ß and IL-18 when overexpressed. We designed experiments to determine whether METH can cause intestinal inflammatory injury via NLRP3 inflammasome overexpression. MATERIAL AND METHODS IEC-6 cells were classified as control, METH (0.5 mM), and METH (0.5 mM)+MCC950 (100 μM) groups. C57BL/6 mice were separated into control, NS, METH (5 mg/kg), and METH (5 mg/kg)+MCC950 (10 mg/kg) groups (n=10). We detected apoptosis, transepithelial electrical resistance (TEER), and proinflammatory factors (IL-6, INF-γ, TNF-alpha, and NF-kappaB) in the METH cell model. We also assessed proinflammatory factors (IL-6, INF-γ, TNF-alpha, and NF-kappaB) and observed intestinal tissues stained with hematoxylin and eosin (HE) in the METH animal model to explore intestinal inflammatory injury due to METH. After adding MCC950 (an NLRP3 inflammasome inhibitor), we additionally detected NLRP3 inflammasome components (NLRP3, Caspase-1, and ASC), IL-1ß, and IL-18 to estimate the relationship of the NLRP3 inflammasome with intestinal inflammatory injury due to METH. RESULTS METH can lead apoptosis, increase proinflammatory factors (e.g., IL-6, INF-γ, TNF-alpha, and NF-kappaB), and decrease TEER in the METH cell model. In the METH animal model, METH can cause obvious injury and increase proinflammatory factors (e.g., IL-6, INF-γ, TNF-alpha, and NF-kappaB). All the intestinal inflammatory changes due to METH depended on overexpression of the NLRP3 inflammasome and could be ameliorated by MCC950, except for ASC and NF-kappaB. CONCLUSIONS METH, in addition to being a confirmed neurotoxic drug, can also cause severe intestinal inflammatory injury via NLRP3 inflammasome overexpression. NF-kappaB may be an activator of the NLRP3 inflammasome in METH intestinal inflammatory injury.
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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.