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Protective Effects of Chlorogenic Acid against Experimental Reflux Esophagitis in Rats

机译:绿原酸对大鼠实验性反流性食管炎的保护作用

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摘要

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-α, 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.
机译:食管胃内容物反流会引起食管粘膜损伤和炎症。最近的研究表明,氧源性自由基在反流性食管炎(RE)中介导粘膜损伤。绿原酸(CGA)是咖啡酸和奎宁酸的酯,是人类饮食中含量最丰富的多酚之一,具有抗炎,抗菌和抗氧化的作用。在这种情况下,我们研究了CGA对大鼠实验性RE的影响。通过在前胃和腺体部分之间的过渡区域结扎并用一小段导管覆盖幽门环附近的十二指肠来产生RE。 RE手术后48小时口服CGA(10、30和100 mg / kg)和奥美拉唑(阳性对照,10 mg / kg),持续12天。 CGA减轻了食道病变的严重程度,这种有益效果已通过组织病理学观察得到证实。 CGA减少了食管脂质过氧化作用,并增加了降低的谷胱甘肽/氧化型谷胱甘肽比率。 CGA减弱了血清中肿瘤坏死因子-α的水平,以及诱导型一氧化氮合酶和环氧合酶-2蛋白的表达。 CGA减轻了RE诱导的粘膜损伤,这种保护作用与降低的氧化应激和CGA的抗炎特性有关。

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