Antiulcerogenic activity of chlorogenic acid in different models of gastric ulcer

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 pre...

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Bibliographic Details
Published in:Naunyn-Schmiedeberg's archives of pharmacology 2013, Vol.386 (1), p.5-14
Main Authors: Shimoyama, André T., Santin, José Roberto, Machado, Isabel D., de Oliveira e Silva, Ana Mara, de Melo, Illana L. Pereira, Mancini-Filho, Jorge, Farsky, Sandra H. P.
Format: Article
Language:English
Subjects:
Animals
Anti-Inflammatory Agents, Non-Steroidal - toxicity
Anti-Ulcer Agents - administration & dosage
Anti-Ulcer Agents - pharmacology
Antioxidants - pharmacology
Biomedical and Life Sciences
Biomedicine
Carbenoxolone - pharmacology
Chlorogenic Acid - administration & dosage
Chlorogenic Acid - pharmacology
Disease Models, Animal
Dose-Response Relationship, Drug
Ethanol - toxicity
Male
Mice
Neurosciences
Omeprazole - pharmacology
Original Article
Pharmacology/Toxicology
Stomach Ulcer - chemically induced
Stomach Ulcer - drug therapy
Stomach Ulcer - pathology
Time Factors
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Summary: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.
ISSN:0028-1298
1432-1912
DOI:10.1007/s00210-012-0807-2