ArticleToxicology international
Protective Effects of Propofol Against Methamphetamine-induced Neurotoxicity.
Article in Toxicology international. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 33 citations in OpenAlex.
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- 5-HT3 antagonist, tropisetron, ameliorates age-related renal injury induced by D-galactose in male mice: Up-regulation of sirtuin 1.Iranian journal of basic medical sciences · 2024Article
- Zinc and selenium supplement mitigated valproic acid-induced testis toxicity by modulating the oxidative redox balance in male rats.Anatomy & cell biology · 2021Article
- Methamphetamine-induced dopaminergic neurotoxicity as a model of Parkinson's disease.Archives of pharmacal research · 2021Review
- Ginkgo biloba attenuated hepatotoxicity induced by combined exposure to cadmium and fluoride via modulating the redox imbalance, Bax/Bcl-2 and NF-kB signaling pathways in male rats.Molecular biology reports · 2020Article
- Co-exposure to non-toxic levels of cadmium and fluoride induces hepatotoxicity in rats via triggering mitochondrial oxidative damage, apoptosis, and NF-kB pathways.Environmental science and pollution research international · 2020Article
- Radioprotective effect of diethylcarbamazine on radiation-induced acute lung injury and oxidative stress in mice.Journal of bioenergetics and biomembranes · 2020Article
- The protective effect of propofol on ionizing radiation-induced hematopoietic system damage in mice.RSC advances · 2019Article
- Tea Polyphenols Attenuate Methamphetamine-Induced Neuronal Damage in PC12 Cells by Alleviating Oxidative Stress and Promoting DNA Repair.Frontiers in physiology · 2019Article
- Role of Mitochondria in Methamphetamine-Induced Dopaminergic Neurotoxicity: Involvement in Oxidative Stress, Neuroinflammation, and Pro-apoptosis-A Review.Neurochemical research · 2018Review
- Atorvastatin attenuates ethanol-induced hepatotoxicity via antioxidant and anti-inflammatory mechanisms.Research in pharmaceutical sciences · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
contextMethamphetamine (METH) is widely abused in worldwide. METH use could damage the dopaminergic system and induce neurotoxicity via oxidative stress and mitochondrial dysfunction. Propofol, a sedative-hypnotic agent, is known for its antioxidant properties. In this study, we used propofol for attenuating of METH-induced neurotoxicity in rats. SUBJECTS AND
methodsWe used Wistar rats that the groups (six rats each group) were as follows: Control, METH (5 mg/kg IP), and propofol (5, 10 and 20 mg/kg, IP) was administered 30 min before METH. After 24 h, animals were killed, brain tissue was separated and the mitochondrial fraction was isolated, and oxidative stress markers were measured.
resultsOur results showed that METH significantly increased oxidative stress markers such as lipid peroxidation, reactive oxygen species formation and glutathione oxidation in the brain, and isolated mitochondria. Propofol significantly inhibited METH-induced oxidative stress in the brain and isolated mitochondria. Mitochondrial function decreased dramatically after METH administration that propofol pretreatment significantly improved mitochondrial function. Mitochondrial swelling and catalase activity also increased after METH exposure but was significantly decreased with propofol pretreatment.
conclusionsThese results suggest that propofol prevented METH-induced oxidative stress and mitochondrial dysfunction and subsequently METH-induced neurotoxicity. Therefore, the effectiveness of this antioxidant should be evaluated for the treatment of METH toxicity and neurodegenerative disease.
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