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目的:研究石榴皮鞣质对动物实验性胃损伤的影响。方法:应用大鼠幽门结扎型胃溃疡模型、大鼠乙醇诱导的胃黏膜损伤模型和小鼠水拘禁应激致胃溃疡模型,观察不同剂量的石榴皮鞣质ig给予对实验性胃损伤的防治作用,对胃黏膜中一氧化氮(NO)和丙二醛(MDA)含量,对谷胱甘肽还原酶(GSH-PX)和超氧化物歧化酶(SOD)活力,对胃液、胃酸、胃黏液和胃蛋白酶分泌的影响。结果:石榴皮鞣质(500,150,50 mg.kg-1)ig给予呈剂量依赖性明显抑制水拘禁应激性小鼠胃溃疡及大鼠幽门结扎型胃溃疡的形成和无水乙醇致胃黏膜损伤的发生,阻遏无水乙醇引起的胃黏膜组织内NO水平下降和MDA生成增加,抑制胃黏膜GSH-PX和SOD活力降低和促进胃黏液的分泌,但对胃液分泌、游离酸度、总酸度和总酸排出量及胃蛋白酶活性无明显影响。结论:石榴皮鞣质对动物实验性胃溃疡具有良好的防治疗作用,这种作用可能与促进胃黏液分泌,维护黏膜屏障的完整性,进而减少自由基生成、降低抗脂质过氧化反应酶的消耗和调控NO水平有关。
Objective: To study the effect of tanned tanned pomegranate extract on experimental gastric lesions in animals. METHODS: Rat model of pylorus-ligated gastric ulcer, ethanol-induced gastric mucosal injury model in rats and mouse model of gastric ulcer induced by water detention were used to observe the prevention and treatment of different doses of guava tannin ig given to experimental gastric lesions. Role of nitric oxide (NO) and malondialdehyde (MDA) in gastric mucosa, activity of glutathione reductase (GSH-PX) and superoxide dismutase (SOD), gastric juice, stomach acid, stomach Effects of mucus and pepsin secretion. RESULTS: The ig was significantly (500, 150, 50 mg.kg-1) in the pomegranate rind dose-dependently inhibited gastric ulcers in stress-induced mice and the formation of pylorus-ligated gastric ulcers in rats and ethanol-induced gastric mucosa. The occurrence of injury inhibited the decrease of NO and the increase of MDA production in gastric mucosa caused by anhydrous ethanol, inhibited the decrease of GSH-PX and SOD activity in gastric mucosa and promoted the secretion of gastric mucus, but the secretion of gastric juice, free acidity, total acidity and Total acid output and pepsin activity had no significant effect. Conclusion: Pomegranate tannin has a good anti-therapeutic effect on experimental gastric ulcers in animals. This effect may be associated with promoting the secretion of gastric mucus and maintaining the integrity of the mucosal barrier, thereby reducing free radical production and reducing the anti-lipid peroxidation enzyme. The consumption is related to the regulation of NO levels.