Antiulcerogenic activity of chlorogenic acid in different models of gastric ulcer
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- 作者：André T. Shimoyama (1)
José Roberto Santin (1)
Isabel D. Machado (1)
Ana Mara de Oliveira e Silva (2)
Illana L. Pereira de Melo (2)
Jorge Mancini-Filho (2)
Sandra H. P. Farsky (1) - 关键词：Neutrophils ; Antioxidant enzymes ; Inflammatory mediators ; Ethanol/HCl solution ; Piroxicam
- 刊名：Naunyn-Schmiedeberg's Archives of Pharmacology
- 出版年：2013
- 出版时间：January 2013
- 年：2013
- 卷：386
- 期：1
- 页码：5-14
- 全文大小：446KB
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José Roberto Santin (1)
Isabel D. Machado (1)
Ana Mara de Oliveira e Silva (2)
Illana L. Pereira de Melo (2)
Jorge Mancini-Filho (2)
Sandra H. P. Farsky (1)
1. Laboratory of Experimental Toxicology, Department of Clinical and Toxicological Analyses, Faculty of Pharmaceutical Sciences, University of S?o Paulo, S?o Paulo, Brazil
2. Department of Food Science, Faculty of Pharmaceutical Science, University of S?o Paulo, S?o Paulo, Brazil - ISSN：1432-1912
文摘
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?μL/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.