BACKGROUND AND AIM: Recently, statins have appeared to have additional benefits beyond their lipid lowering effects, which has led to the interest in the use of this class of drugs outside the realm of cardiovascular disease. Simvastatin (SIM) is a commonly prescribed statin with anti-inflammatory and antioxidant properties. Excessive generation of oxygen-derived free radicals (ODFR) and proinflammatory mediators has been implicated in the pathogenesis of gastric ulcers. This investigation aimed to study the effect of SIM on experimentally induced gastric acid secretion and ulcer formation. METHODS: Adult Wistar rats were divided into experimental groups containing six animals. Acid secretion studies were undertaken using pylorus-ligated rats pretreated with SIM (20, 40, and 60 mg/kg). The effect of orally administered SIM was also studied on indomethacin- and ethanol-induced gastric ulcers. The levels of myeloperoxidase (MPO), non-protein sulfhydryls (NP-SH), nitric oxide (NO), antioxidant enzymes, and gastric wall mucus were measured in the glandular stomach of rats following ethanol-induced gastric lesions. RESULTS: Administration of SIM significantly and dose-dependently inhibited the volume of gastric secretion and the acidity. Pretreatment with SIM significantly reduced the formation of indomethacin- and ethanol-induced gastric lesions. The antiulcer activity of SIM was associated with significant attenuation of adverse effects of ethanol on gastric wall mucus, NP-SH and MPO. SIM modified the gastric NO levels and reversed the ethanol-induced decrease in glutathione-S-transferase and increase in superoxide dismutase and catalase. CONCLUSIONS: These findings clearly suggest the involvement of proinflammatory agents and ODFR in the pathogenesis of gastric lesions. The gastroprotective effects of SIM are mediated by inhibition of neutrophils activity, reduction of oxidative stress, and maintenance of vascular integrity. This study was conducted in rats; its relevance to human gastric ulcers is not known and warrants further study.
BACKGROUND AND AIM: Recently, statins have appeared to have additional benefits beyond their lipid lowering effects, which has led to the interest in the use of this class of drugs outside the realm of cardiovascular disease. Simvastatin (SIM) is a commonly prescribed statin with anti-inflammatory and antioxidant properties. Excessive generation of oxygen-derivedfree radicals (ODFR) and proinflammatory mediators has been implicated in the pathogenesis of gastric ulcers. This investigation aimed to study the effect of SIM on experimentally induced gastric acid secretion and ulcer formation. METHODS: Adult Wistar rats were divided into experimental groups containing six animals. Acid secretion studies were undertaken using pylorus-ligated rats pretreated with SIM (20, 40, and 60 mg/kg). The effect of orally administered SIM was also studied on indomethacin- and ethanol-induced gastric ulcers. The levels of myeloperoxidase (MPO), non-protein sulfhydryls (NP-SH), nitric oxide (NO), antioxidant enzymes, and gastric wall mucus were measured in the glandular stomach of rats following ethanol-induced gastric lesions. RESULTS: Administration of SIM significantly and dose-dependently inhibited the volume of gastric secretion and the acidity. Pretreatment with SIM significantly reduced the formation of indomethacin- and ethanol-induced gastric lesions. The antiulcer activity of SIM was associated with significant attenuation of adverse effects of ethanol on gastric wall mucus, NP-SH and MPO. SIM modified the gastric NO levels and reversed the ethanol-induced decrease in glutathione-S-transferase and increase in superoxide dismutase and catalase. CONCLUSIONS: These findings clearly suggest the involvement of proinflammatory agents and ODFR in the pathogenesis of gastric lesions. The gastroprotective effects of SIM are mediated by inhibition of neutrophils activity, reduction of oxidative stress, and maintenance of vascular integrity. This study was conducted in rats; its relevance to humangastric ulcers is not known and warrants further study.
Authors: Abdulrahman Al Asmari; Saud Al Omani; Malfi Al Otaibi; Abdul-Aziz Al Abdulaaly; Ibrahim Elfaki; Khalid Al Yahya; Mohammed Arshaduddin Journal: Int J Clin Exp Med Date: 2014-03-15
Authors: Abdulrahman Al Asmari; Mohammed Arshaduddin; Ibrahim Elfaki; Saeed Kadasah; Abdulrahman Al Robayan; Saeed Al Asmary Journal: Int J Clin Exp Med Date: 2014-08-15
Authors: Nathalia S Carvalho; Mônica M Silva; Renan O Silva; Lucas A D Nicolau; Thiago S L Araújo; Douglas S Costa; Nayara A Sousa; Luan K M Souza; Pedro M G Soares; Jand Venes R Medeiros Journal: Dig Dis Sci Date: 2015-09-24 Impact factor: 3.199
Authors: Felipe Meira de-Faria; Ana Cristina Alves Almeida; Anderson Luiz-Ferreira; Christiane Takayama; Ricardo José Dunder; Marcelo Aparecido da Silva; Marcos José Salvador; Patrícia Verardi Abdelnur; Marcos Nogueira Eberlin; Wagner Vilegas; Walber Toma; Alba Regina Monteiro Souza-Brito Journal: ScientificWorldJournal Date: 2012-04-30
Authors: Mohd Fahami Nur Azlina; Yusof Kamisah; Kien Hui Chua; Ibrahim Abdel Aziz Ibrahim; Hj Mohd Saad Qodriyah Journal: PLoS One Date: 2015-10-14 Impact factor: 3.240
Authors: Anderson Luiz-Ferreira; Maira Cola; Victor Barbastefano; Felipe Meira de-Faria; Ana Beatriz A de Almeida; Elisângela Farias-Silva; Tamara Regina Calvo; Clélia A Hiruma-Lima; Wagner Vilegas; Alba Regina M Souza-Brito Journal: Int J Mol Sci Date: 2012-11-15 Impact factor: 5.923