title: N-acetylcysteine a possible protector against indomethacin-induced peptic ulcer: crosstalk between antioxidant, anti-inflammatory, and antiapoptotic mechanisms.
abstract: This study investigated the gastroprotective effects of N-acetylcysteine (NAC) against indomethacin-induced gastric ulcer in rats. Ulceration was induced by a single oral administration of indomethacin (30 mg/kg). 50 male albino rats were allocated into 5 equal groups: control group received normal saline orally, indomethacin group rats received normal saline orally for 5 days and indomethacin (50 mg/kg) on the last day, ranitidine group received ranitidine (reference drug) orally for 5 days (50 mg/kg) before receiving indomethacin (50 mg/kg) on the last day, and NAC groups received NAC orally at 300 and 500 mg/kg, respectively, for 5 days before receiving indomethacin (50 mg/kg) on the last day. Gastric tissue interleukin-1β (IL-1β), interferon-γ (IFN-γ), and caspase-3 levels were immunoassayed. Total thiol (T-SH), myeloperoxidase (MPO), and glucose-6-phosphate dehydrogenase (G6PD) were determined by spectrophotometry. Cytokine-induced neutrophil chemoattractant 2α (CINC-2α) gene expression was evaluated in addition to Bcl-2 immunohistochemistry. Pretreatment with NAC improved the inflammatory, apoptotic, and redox status in a dose-dependent manner particularly in NAC 500 mg/kg pretreated group. These results show a role for NAC in improving indomethacin-induced gastric ulceration via antioxidative, antiapoptotic, and anti-inflammatory interactive mechanisms.
authors.affiliation: a Department of Medical Biochemistry, Faculty of Medicine, Tanta University, Tanta, Egypt.
authors.forename: Nema Ali
authors.initials: NA
authors.lastname: Soliman
authors.affiliation: a Department of Medical Biochemistry, Faculty of Medicine, Tanta University, Tanta, Egypt.
authors.forename: Doaa Hussein
authors.initials: DH
authors.lastname: Zineldeen
authors.affiliation: b Department of Pharmacology and Toxicology, Faculty of Pharmacy, Damanhur University, Damanhur, Egypt.
authors.forename: Mohamed Alaa
authors.initials: MA
authors.lastname: Katary
authors.affiliation: c Department of Histopathology, Faculty of Medicine, Tanta University, Tanta, Egypt.
authors.forename: Darin Abd
authors.initials: DA
authors.lastname: Ali
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000009:adverse effects / Q000627:therapeutic use; D000975:Antioxidants / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000378:metabolism; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology; D019743:Chemokines, CXC / Q000378:metabolism; D019610:Cytoprotection; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005753:Gastric Mucosa / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D006801:Humans; D007213:Indomethacin / Q000009:adverse effects; D007371:Interferon-gamma / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D008297:Male; D010084:Oxidation-Reduction / Q000187:drug effects*; D010146:Pain / Q000188:drug therapy; D009195:Peroxidase / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D011899:Ranitidine / Q000009:adverse effects / Q000627:therapeutic use; D051381:Rats; D017208:Rats, Wistar; D013276:Stomach Ulcer / Q000139:chemically induced / Q000517:prevention & control*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000897:Anti-Ulcer Agents; D000975:Antioxidants; C000617196:Bcl2 protein, rat; D019743:Chemokines, CXC; C513294:Cxcl3 protein, rat; D053583:Interleukin-1beta; D019253:Proto-Oncogene Proteins c-bcl-2; D007371:Interferon-gamma; D011899:Ranitidine; D005954:Glucosephosphate Dehydrogenase; D009195:Peroxidase; D053148:Caspase 3; D000111:Acetylcysteine; D007213:Indomethacin
keywords: N-acetylcysteine; N-acétyl cysteine; Peptic ulcer; apoptose; apoptosis; cytokine-induced neutrophil chemoattractant 2α; cytokines; ulcère peptique; « cytokine-induced neutrophil chemoattractant 2α »