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目的探讨三叶因子2(TFF2)基因治疗对实验性大鼠胃溃疡的疗效及其机制。方法2005-06-10—2006-03-15南方医科大学南方医院消化病研究所将48只雄性Wistar大鼠随机分为2组,治疗组24只,对照组24只。治疗组每只应用pcDNA3.1g+TFF2100μg,对照组每只应用等容积pcDNA3.1g+TFF2100μg,均在造模时经胃壁浆膜下注入。用药后分别在第3、7、14天处死动物,测量大鼠胃溃疡指数、胃总酸度及黏液糖蛋白量的变化。结果在应用pcDNA3.1g+TFF2的第3天,治疗组和对照组比较,各项指标差异无统计学意义(P>0.05);第7天,治疗组的黏液糖蛋白量显著增加,与对照组比较差异有统计学意义(P<0.01)。第14天,治疗组的溃疡面积显著缩小,与对照组比较差异有统计学意义(P<0.01);治疗组黏液糖蛋白量有所下降,不过与对照组比较差异也有统计学意义(P<0.05);而治疗组的胃总酸度变化不大,与对照组比较差异无统计学意义(P>0.05)。结论TFF2基因治疗对实验性大鼠胃溃疡愈合有促进作用,增加胃黏液糖蛋白的分泌是其促进溃疡愈合的机制之一,而与抑制胃酸分泌无关。
Objective To investigate the therapeutic effect and mechanism of trefoil factor 2 (TFF2) gene therapy on experimental gastric ulcer in rats. Methods Southern Institute of Digestive Diseases, Southern Medical University 48 male Wistar rats were randomly divided into two groups, 24 in the treatment group and 24 in the control group. The treatment group, each application of pcDNA3.1g + TFF2100μg, the control group each application of equal volume of pcDNA3.1g + TFF2100μg, all in the modeling by the sub-gastric wall injection. The animals were sacrificed on the 3rd, 7th and 14th day after the treatment, and the changes of gastric ulcer index, total gastric acidity and mucus glycoprotein in rats were measured. Results On the third day after application of pcDNA3.1g + TFF2, there was no significant difference between the treatment group and the control group (P> 0.05). On the seventh day, the mucosal glycoprotein of the treatment group increased significantly, The difference was statistically significant (P <0.01). On the fourteenth day, the ulcer area of the treatment group was significantly reduced compared with that of the control group (P <0.01); the amount of mucus glycoprotein in the treatment group was decreased, but the difference was statistically significant compared with the control group (P < 0.05). There was no significant difference in the total acidity of the stomach between the treatment group and the control group (P> 0.05). Conclusion TFF2 gene therapy can promote the healing of experimental gastric ulcer in rats. Increasing the secretion of gastric mucosal glycoprotein is one of the mechanisms that promote the healing of ulcer, but not the inhibition of gastric acid secretion.