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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Antiulcerogenic activity of chlorogenic acid in different models of gastric ulcer

Texto completo
Autor(es):
Shimoyama, Andre T. [1] ; Santin, Jose Roberto [1] ; Machado, Isabel D. [1] ; de Oliveira e Silva, Ana Mara [2] ; Pereira de Melo, Illana L. [2] ; Mancini-Filho, Jorge [2] ; Farsky, Sandra H. P. [1]
Número total de Autores: 7
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Fac Pharmaceut Sci, Lab Expt Toxicol, Dept Clin & Toxicol Anal, Sao Paulo - Brazil
[2] Univ Sao Paulo, Fac Pharmaceut Sci, Dept Food Sci, Sao Paulo - Brazil
Número total de Afiliações: 2
Tipo de documento: Artigo Científico
Fonte: NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY; v. 386, n. 1, p. 5-14, JAN 2013.
Citações Web of Science: 33
Resumo

Chlorogenic acid (CGA) is found in many foods, including coffee, berries, potatoes, carrots, wine, apples, and various herbs, and has anti-inflammatory, antidiabetic, and antitumoral actions. The CGA is well absorbed orally, and its effects on gastric ulcer have not been previously reported. The present manuscript evaluated the effect of oral administration of CGA on ethanol/HCl (Et/HCl) or nonsteroidal anti-inflammatory drug (NSAID)-induced gastric ulcer model in male Swiss mice. Animals were pretreated with 0.2 % carboxymethylcellulose (vehicle, p.o.), omeprazole (positive control, 30 mg/kg, p.o.), carbenoxolone (antioxidant positive control, 100 mg/kg, p.o.), or CGA (5, 25, or 50 mg/kg, p.o.). One hour later, the gastric ulcer was induced by injecting Et/HCl solution (100 mu L/10 g body weight; Et 60 % + HCl 0.03 M) or piroxicam (100 mg/kg, p.o). After another hour or 4 h later, gastric tissues were collected from Et/HCl or piroxicam-treated animals, respectively, to evaluate the size of the lesion, histological alterations, secretion of gastric acid, neutrophil migration, oxidative/antioxidative enzymes, markers of lipid peroxidation, or concentrations of inflammatory mediators. CGA treatment had a gastroprotective effect in both models, reducing the percentage of lesioned area. CGA treatment did not alter the secretion of gastric action but inhibited neutrophil migration and restored the levels of catalase, superoxide dismutase, glutathione peroxidase, glutathione, and thiobarbituric acid reactive substances in mice treated with Et/HCl. Additionally, CGA treatment blocked the increase of tumor necrosis factor alpha and leukotriene B4 but did not restore the reduced prostaglandin levels in the NSAID-induced ulcer. Together, the data presented herein show that CGA may be a suitable natural compound for the prevention and treatment of gastric lesions caused by a different etiology. (AU)

Processo FAPESP: 11/01848-8 - Avaliação da atividade gastroprotetora do agonista PPAR Lyso-07 e do ácido clorogênico
Beneficiário:Sandra Helena Poliselli Farsky
Modalidade de apoio: Auxílio à Pesquisa - Regular
Processo FAPESP: 10/18069-9 - Avaliação da atividade gastroprotetora do ácido clorogênico em úlceras gástricas induzidas em ratos
Beneficiário:André Tominaga Shimoyama
Modalidade de apoio: Bolsas no Brasil - Iniciação Científica