title: Hepatoprotective effect of methylsulfonylmethane against carbon tetrachloride-induced acute liver injury in rats.
abstract: This study evaluated the effect of methylsulfonylmethane (MSM) on carbon tetrachloride (CCl₄)-induced acute liver injury in rats. A single injection of CCl₄ (2 ml/kg, i.p.) increased serum aminotransferases (ALT and AST) activities. In addition, CCl₄ treatment led to elevation of hepatic malondialdehyde (MDA) content as well as decrease in superoxide dismutase (SOD) and catalase (CAT) activities. Furthermore, cytochrome P450 2E1 (CYP2E1) content was suppressed while proinflammatory cytokines tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels increased in liver tissue after CCl4 administration. We showed that acute CCl₄-induced damage was accompanied by a rise in Bax/Bcl₂ ratio indicating apoptosis. Pre-treatment with MSM (400 mg/kg) inhibited the increases of serum ALT and AST activities, decreased hepatic MDA, TNF-α, IL-6 and Bax/Bcl₂ ratio compared to CCl₄ treated group. On the other hand, MSM raised SOD and CAT activities as well as CYP2E1 level in liver tissues. The present study shows that MSM possesses a hepatoprotective effect against CCl₄-induced liver injury in rats. This protective effect might be through its antioxidant, anti-inflammatory and antiapoptotic properties.
authors.affiliation: Department of Pharmacology and Toxicology, Faculty of Pharmacy, Helwan University, Ein Helwan, Cairo, Egypt, kamelrehab@yahoo.com.
authors.forename: Rehab
authors.initials: R
authors.lastname: Kamel
authors.forename: Engy M
authors.initials: EM
authors.lastname: El Morsy
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects; D051017:Apoptosis Regulatory Proteins / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D002252:Carbon Tetrachloride Poisoning / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D002374:Catalase / Q000737:chemistry / Q000378:metabolism; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology / Q000517:prevention & control*; D019392:Cytochrome P-450 CYP2E1 / Q000378:metabolism; D065691:Cytochrome P-450 CYP2E1 Inhibitors; D016207:Cytokines / Q000819:agonists / Q000378:metabolism; D004121:Dimethyl Sulfoxide / Q000627:therapeutic use*; D005260:Female; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D020011:Protective Agents / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013450:Sulfones / Q000627:therapeutic use*; D013482:Superoxide Dismutase / Q000737:chemistry / Q000378:metabolism
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D051017:Apoptosis Regulatory Proteins; D015415:Biomarkers; D065691:Cytochrome P-450 CYP2E1 Inhibitors; D016207:Cytokines; D020011:Protective Agents; D013450:Sulfones; D008315:Malondialdehyde; C025910:dimethyl sulfone; D002374:Catalase; D019392:Cytochrome P-450 CYP2E1; D013482:Superoxide Dismutase; D004121:Dimethyl Sulfoxide