Anti-ulcerogenic effect of chitin and chitosan on mucosal antioxidant defence system in HCl-ethanol-induced ulcer in rats
Anti-ulcerogenic effect of chitin and chitosan on mucosal antioxidant defence system in HCl-ethanol-induced ulcer in rats
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DOI：
10.1211/0022357023079
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发表时间：
2004-02-01
影响因子：
3.3
通讯作者：
Mathew, S
中科院分区：
文献类型：
--
作者：
Anandan, R;Nair, PGV;Mathew, S
研究了几丁质和壳聚糖对盐酸乙醇诱导的雄性Wistar大鼠溃疡的抑制作用。测定正常组和实验组大鼠胃黏膜酸排泄量、胃蛋白酶、蛋白质、脂质过氧化物和还原性谷胱甘肽水平，以及谷胱甘肽过氧化物酶（GPx）、谷胱甘肽s转移酶（GST）、过氧化氢酶（CAT）和超氧化物歧化酶（SOD）活性。溃疡诱导组大鼠胃液体积和酸度显著增加。与正常对照组相比，消化酶活性明显降低。2%甲壳素和壳聚糖随饲料预处理大鼠胃黏膜体积、泌酸量和消化酶活性维持在接近正常水平。与正常对照组相比，溃疡黏膜的脂质过氧化水平明显升高。这与溃疡诱导大鼠胃粘膜还原性谷胱甘肽水平和抗氧化酶如GPx、GST、CAT和SOD活性的下降相一致。此外，粘膜蛋白和糖蛋白成分的水平在溃疡粘膜中显著减少。几丁质和壳聚糖预处理对盐酸乙醇诱导的大鼠溃疡均有明显的抑制作用。
The anti-ulcerogenic effect of chitin and chitosan against ulcer induced by HCl-ethanol in male Wistar rats was studied. Levels of acid output, pepsin, protein, lipid peroxides and reduced glutathione and the activity of glutathione peroxidase (GPx), glutathione-S-transferase (GST), catalase (CAT) and superoxide dismutase (SOD) were determined in the gastric mucosa of normal and experimental groups of rats. A significant increase in volume and acidity of the gastric juice was observed in the ulcer-induced group of rats. Peptic activity was significantly decreased as compared with that of normal controls. In the rats pre-treated with chitin and chitosan 2% along with feed, the volume and acid output and peptic activity of gastric mucosa were maintained at near normal levels. The level of lipid peroxidation was significantly higher in the ulcerated mucosa when compared with that of normal controls. This was paralleled by a decline in the level of reduced glutathione and in the activity of antioxidant enzymes like GPx, GST, CAT and SOD in the gastric mucosa of ulcer-induced rats. Also, the levels of mucosal proteins and glycoprotein components were significantly depleted in ulcerated mucosa. The pre-treatment with chitin and chitosan was found to exert a significant anti-ulcer effect by preventing all the HCl-ethanol-induced ulcerogenic effects in experimental rats.