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[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 protective mechanism of carboxymethyl chitosan on acetic acid-type gastric ulcer in rats. [Methods] Forty SD rats were randomly divided into four groups (n = 10): normal group, model group, sucralfate group and carboxymethyl chitosan group. Chronic gastric ulcer model was established by subretinal injection with 20% acetic acid and 0.05 ml subcutaneously. After 3 days of modeling, gavage administration was given. After 14 days, the ulcer area of each group was calculated. Immunohistochemical staining and reverse transcription polymerase chain The mRNA and protein levels of Bcl-2 in gastric mucosal cells were detected by RT-PCR. [Results] Compared with the model group, the area of gastric ulcer induced by acetic acid decreased after treatment with carboxymethyl chitosan and sucralfate, and the protein and mRNA expression of Bcl-2 increased. [Conclusion] Carboxymethyl chitosan may accelerate the ulcer healing by decreasing the apoptosis of gastric mucosal epithelial cells.