ArticleIranian journal of pharmaceutical research : IJPR2014
Propofol Attenuates Toxic Oxidative Stress by CCl4 in Liver Mitochondria and Blood in Rat.
Article in Iranian journal of pharmaceutical research : IJPR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 23 citations in OpenAlex.
- Anesthetic-mediated cardioprotection: from molecular mechanisms to clinical translation challenges.Frontiers in physiology · 2025Review
- Renoprotective and Cardioprotective Potential ofEvidence-based complementary and alternative medicine : eCAM · 2022Article
- Tribulus terrestris ameliorates carbon tetrachloride-induced hepatotoxicity in male rats through suppression of oxidative stress and inflammation.Environmental science and pollution research international · 2020Article
- The potential protective effect of two actinomycete extracts against carbon tetrachloride-induced hepatotoxicity in rats.Environmental science and pollution research international · 2019Article
- Propofol attenuates sepsis-induced acute kidney injury by regulating miR-290-5p/CCL-2 signaling pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018Article
- Preventive activity of banana peel polyphenols on CClExperimental and therapeutic medicine · 2016Article
- In vivo study of hepatic oxidative stress and mitochondrial function in rabbits with severe hypotension after propofol prolonged infusion.SpringerPlus · 2016Article
- Protective Effects of Propofol Against Methamphetamine-induced Neurotoxicity.Toxicology internationalArticle
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anti-oxidant effects of propofol (2, 6-diisopropylphenol) were evaluated agains carbon tetrachloridet CCl4 -induced oxidative stress in rat liver. 30 male rats were equally divided in to 6 groups (5 rats each). Group I (control), while Group II was given CCl4 (3 mL /Kg/day, IP). Animals of Groups III received only propofol (10 mg/Kg/day, IP). Group IV was given propofol+ CCl4. Group V was administered vitamin E (alpha-tocopherol acetate 15 mg/Kg/day, SC) .Animals of Group VII received alpha-tocopherol acetate + CCl4 once daily for two weeks. After treatment, blood and liver mitochondria were isolated. Anti-oxidant enzymes activity such as glutathione peroxidase (GPx), superoxide dismutase (SOD) and oxidative stress marker such as reduced glutathione (GSH) and lipid peroxidation (LPO) concentration were measured. Oxidative stress induced with CCl4 in liver mitochondria was evident by a significant increase in enzymatic activities of GPx, SOD, and LPO and decreased of GSH and vailability of mitochondria. Propofol and vitamin E restored CCl4-induced changes in GSH, GPx, SOD and LPO in blood and liver mitochondria. CCl4 decreased viability of mitochondria that was recovered by propofol and vitamin E. It is concluded that oxidative damage is the mechanism of toxicity of CCl4 in the mitochondria that can be recovered by propofol comparable to vitamin E.
Indexed as
Identifiers
24734078PMC3985254W1953242687What OpenQuestion holds
Registered trials
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