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作 者:赵健亚 吴金彪 陆颖[1] 仇梁林[1] 周松林[1] 徐广飞[1]
机构地区:[1]南通大学公共卫生学院营养与食品卫生学教研室,南通226001 [2]宁波市检验检疫局
出 处:《现代预防医学》2010年第9期1626-1628,共3页Modern Preventive Medicine
基 金:南通大学自然科学研究项目(06Z106)
摘 要:[目的]探讨羧甲基壳聚糖对大鼠乙酸型胃溃疡的保护作用机制。[方法]40只SD大鼠随机分为4组,每组10只,分别为正常组、模型组、硫糖铝组和羧甲基壳聚糖组。用20%乙酸0.05ml浆膜下注射法建立大鼠慢性胃溃疡模型,造模3d后开始灌胃给药,连续14d后计算各组溃疡面积,用免疫组化染色法和逆转录聚合酶链反应(RT-PCR)检测胃黏膜细胞中Bcl-2基因蛋白和mRNA表达水平。[结果]与模型组相比,羧甲基壳聚糖和硫糖铝治疗后,乙酸诱导的胃溃疡面积缩小;Bcl-2基因蛋白和mRNA表达水平均增加。[结论]羧甲基壳聚糖可能通过减少胃黏膜上皮细胞的凋亡,加速溃疡愈合。[Objective] To investigate the mechanism of Carboxymethyl-chitosan (CM-Chitosan) against acetic acid-induced chronic gastric ulcers in rats. [Methods] 40 Sprague-Dawley rats were randomly divided into normal group, model group, sucralfate group and CM-chitosan group. The rat models of chronic gastric ulcers were established by injecting 20% acetic acid 0.05ml into gastric mucosa. 14 days after the intragastric administration, rats were killed. The ulcer area was measured, and the expressions of Bcl-2 protein and mRNA in gastric mucosa were detected by immunohistochemical staining and RT-PCR, respectively. [Results] CM-chitosan reduced the ulcer area of ulcer rats induced by acetic acid and increased the expression of Bcl-2 protein and mRNA in gastric mucosa. [Conclusion] Our results suggest that CM-chitosan might accelerate the healing of gastric ulcer by reducing epithelial cell apoptosis.
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