Protective Effects of Chlorogenic Acid against Experimental Reflux Esophagitis in Rats.
10.4062/biomolther.2014.066
- Author:
Jung Woo KANG
1
;
Sun Mee LEE
Author Information
1. School of Pharmacy, Sungkyunkwan University, Suwon 440-746, Republic of Korea. sunmee@skku.edu
- Publication Type:Original Article
- Keywords:
Chlorogenic acid;
Gastroesophageal reflux disease;
Inflammation;
Oxidative stress;
Reflux esophagitis
- MeSH:
Animals;
Catheters;
Chlorogenic Acid*;
Cyclooxygenase 2;
Diet;
Duodenum;
Esophagitis, Peptic*;
Free Radicals;
Gastroesophageal Reflux;
Glutathione;
Humans;
Inflammation;
Lipid Peroxidation;
Nitric Oxide Synthase Type II;
Omeprazole;
Oxidative Stress;
Polyphenols;
Pylorus;
Quinic Acid;
Rats*;
Tumor Necrosis Factor-alpha
- From:Biomolecules & Therapeutics
2014;22(5):420-425
- CountryRepublic of Korea
- Language:English
-
Abstract:
Esophageal reflux of gastric contents causes esophageal mucosal damage and inflammation. Recent studies show that oxygen-derived free radicals mediate mucosal damage in reflux esophagitis (RE). Chlorogenic acid (CGA), an ester of caffeic acid and quinic acid, is one of the most abundant polyphenols in the human diet and possesses anti-inflammatory, antibacterial and anti-oxidant activities. In this context, we investigated the effects of CGA against experimental RE in rats. RE was produced by ligating the transitional region between the forestomach and the glandular portion and covering the duodenum near the pylorus ring with a small piece of catheter. CGA (10, 30 and 100 mg/kg) and omeprazole (positive control, 10 mg/kg) were administered orally 48 h after the RE operation for 12 days. CGA reduced the severity of esophageal lesions, and this beneficial effect was confirmed by histopathological observations. CGA reduced esophageal lipid peroxidation and increased the reduced glutathione/oxidized glutathione ratio. CGA attenuated increases in the serum level of tumor necrosis factor-alpha, and expressions of inducible nitric oxide synthase and cyclooxygenase-2 protein. CGA alleviates RE-induced mucosal injury, and this protection is associated with reduced oxidative stress and the anti-inflammatory properties of CGA.
