ArticleNeurochemical research2015
Melatonin Protects Methamphetamine-Induced Neuroinflammation Through NF-κB and Nrf2 Pathways in Glioma Cell Line.
Article in Neurochemical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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
26 citing papers in PubMed, 54 citations in OpenAlex.
- Nrf2 Deficiency Exacerbates Methamphetamine-Induced Neuronal Apoptosis and Cognitive Dysfunction in Male Mice.International journal of molecular sciences · 2026Article
- Methamphetamine-Driven Neuroinflammation and Parkinson's Disease Pathology: Mechanistic Insight into Nrf2 and NFĸB Signaling.Molecular neurobiology · 2026Review
- Comprehension of the Function of Antioxidants in Targeting Different Signaling Pathways to Cure Oxidative Stress-induced Hepatotoxicity.Current topics in medicinal chemistry · 2026Review
- Nrf2/Keap1/ARE regulation by plant secondary metabolites: a new horizon in brain tumor management.Cell communication and signaling : CCS · 2024Review
- Illicit Drugs in Surface Waters: How to Get Fish off the Addictive Hook.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Targeting ferroptosis opens new avenues in gliomas.International journal of biological sciences · 2024Review
- p-Nrf2/HO-1 Pathway Involved in Methamphetamine-induced Executive Dysfunction through Endoplasmic Reticulum Stress and Apoptosis in the Dorsal Striatum.Neurotoxicity research · 2023Article
- α-Pinene Attenuates Methamphetamine-Induced Conditioned Place Preference in C57BL/6 Mice.Biomolecules & therapeutics · 2023Article
- Melatonin: a potential therapeutic approach for the management of primary Sjögren's syndrome.Immunologic research · 2023Review
- Melatonin reduces IL-33 and TSLP expression in human nasal epithelial cells by scavenging ROS directly.Immunity, inflammation and disease · 2023Article
- Potential Therapeutic Approach of Melatonin against Omicron and Some Other Variants of SARS-CoV-2.Molecules (Basel, Switzerland) · 2022Review
- The Role of NRF2/KEAP1 Pathway in Glioblastoma: Pharmacological Implications.Medical oncology (Northwood, London, England) · 2022Review
- The Crosstalk Between Neurons and Glia in Methamphetamine-Induced Neuroinflammation.Neurochemical research · 2022Review
- Potential Effects of Nrf2 in Exercise Intervention of Neurotoxicity Caused by Methamphetamine Oxidative Stress.Oxidative medicine and cellular longevity · 2022Review
- Multi-omics landscape of circadian rhythm pathway alterations in Glioma.Bioengineered · 2021Article
- Review
- Role of Melatonin on Virus-Induced Neuropathogenesis-A Concomitant Therapeutic Strategy to Understand SARS-CoV-2 Infection.Antioxidants (Basel, Switzerland) · 2021Review
- An Update on Antioxidative Stress Therapy Research for Early Brain Injury After Subarachnoid Hemorrhage.Frontiers in aging neuroscience · 2021Review
- Role and Therapeutic Potential of Melatonin in the Central Nervous System and Cancers.Cancers · 2020Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methamphetamine (METH) is known as a toxin for neuronal and glial cells. Previous studies have found that METH-induced glial cell death and inflammation is mediated by oxidative stress. However, the exact mechanisms of the inflammatory response remain unclear. Therefore, we hypothesized that the activation of nuclear factor-κB (NF-κB) signaling, a key mediator of inflammation, and the inhibition of nuclear factor erythroid 2-related factor-2 (Nrf2) signaling, a regulator of the antioxidant response, would be significant events occurring in response to METH-induced inflammation in a rat glioma cell line (C6 cells). Our results show that METH increased the production of nitric oxide (NO) and up-regulated the expression of its main regulatory protein, inducible nitric oxide synthase (iNOS). METH also induced NF-κB activation by increasing inhibitory κBα (IκBα) degradation and translocation of the NF-κB (p65) subunit into the nucleus. Additionally, METH inhibited the activation of the Nrf2 pathway by decreasing the translocation of Nrf2 into the nucleus and also by suppressing the expression of heme oxygenase-1 (HO-1), NAD(P)H quinone oxidoreductase-1 (NQO-1), and glutamate-cysteine ligase catalytic subunit (γ-GCLC), resulting in the suppression of superoxide dismutase (SOD) activity. Pretreatment with melatonin effectively promoted Nrf2 activation and reversed the METH-induced NF-κB response. Melatonin increased the expression of HO-1, NQO-1, and γ-GCLC, resulting in increased SOD activity. In addition, melatonin also decreased IκBα degradation, translocation of the p65 subunit, and expression of iNOS, resulting in decreased NO production. Taken together, our results indicate that melatonin diminishes the proinflammatory mediator in METH-stimulated C6 cells by inhibiting NF-κB activation and inducing Nrf2-mediated HO-1, NQO-1, and γ-GCLC expression.
Indexed as
Identifiers
What 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.