Antiulcerogenic activity of chlorogenic acid in different models of gastric ulcer

Author(s)

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]

Affiliation

^[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

• Document type: Journal article
• Source: NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY; v. 386, n. 1, p. 5-14, JAN 2013.
• Web of Science Citations: 33

Abstract

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)

• FAPESP's process: 11/01848-8 - Evaluation of gastroprotective activity of PPAR agonist Lyso-07 and chlorogenic acid
• Grantee: Sandra Helena Poliselli Farsky
• Support Opportunities: Regular Research Grants
• FAPESP's process: 10/18069-9 - Evaluation of the gastroprotective activity of chlorogenic acid in gastric ulcers induced in rats
• Grantee: André Tominaga Shimoyama
• Support Opportunities: Scholarships in Brazil - Scientific Initiation