健胃消胀合剂对慢性萎缩性胃炎模型大鼠TGF-α、COX-2mRNA表达的影响

摘要

目的:观察健胃消胀合剂对慢性萎缩性胃炎模型大鼠胃黏膜转化生长因子 α(TGF-α)、环氧合酶2(COX-2)mRNA表达的影响.方法:用甲基硝基亚硝基胍(MNNG)治疗慢性萎缩性胃炎大鼠模型,36只健康雄性(清洁级)Wistar大鼠随机分为病理模型组、健胃消胀合剂组、摩罗丹对照组,共3组,每组12只.实时定量PCR方法观察健胃消胀合剂对实验性慢性萎缩性胃炎大鼠模型胃黏膜TGF-α、COX-2 mRNA表达的影响,对后者进行图像分析及统计学处理.结果:健胃消胀合剂与摩罗丹均能改善胃黏膜的病理形态,但以健胃消胀合剂效果为佳,经健胃消胀合剂治疗后胃黏膜各层结构基本正常,黏膜固有腺体丰富排列较规则,无明显数量减少.TGF-α、COX-2 mRNA表达健胃消胀合剂组和摩罗丹组与病理模型组比较,差异有统计学意义(P<0.05);健胃消胀合剂组与摩罗丹对照组比较,差异也有统计学意义(P<0.05).结论:健胃消胀合剂可通过增加胃黏膜TGF-αmRNA表达,降低胃黏膜COX-2 mRNA表达而起到治疗慢性萎缩性胃炎的作用.%Objective: To observe the effects of JianWei XiaoZhang mixture on the expressions of gastric mu-cosa transforming growth factor alpha (TGF-α) mRNA, and cyclooxygenase-2 (COX-2) mRNA in rat model with chronic atrophic gastritis. Methods: Rat models with chronic atrophic gastritis were treated with N-Methyl-N'-ni-tro-N-nitrosoguanidine(MNNG). Thirty-six male healthy Wistar rats (clean grade) were randomly divided into patho-logical model group, JianWei XiaoZhang mixture group and the control group of MoLuoDan, three groups totally. Real-time quantitative PCR was performed to observe effects of JianWei XiaoZhang mixture on the expressions of TGF-α and COX-2mRNA in experimental rat models with chronic atrophic gastritis, and image analysis and statisti-cal processing were performed for the later. Results: JianWei XiaoZhang mixture and MoLuoDan both could improve the pathological morphology of gastric mucosa, but JianWei XiaoZhang mixture had better effects. After treating with JianWei XiaoZhang mixture, gastric mucosa structure became almost normal, the arrangement of the inner gland of the mucosa became more abundant without significant decrease in the number. Compared the expressions of TGF-α and COX-2 mRNA of JianWei XiaoZhang mixture and MoLuoDan group with that of pathological model group, the differences were statistically significant (P<0.05); and compared JianWei XiaoZhang mixture group with MoLuoDan group, the differences were also statistically significant (P<0.05). Conclusion: JianWei XiaoZhang mix-ture can take therapeutic effects on CAG through improving the expressions of gastric mucosa TGF-α mRNA and re-straining the expression of gastric mucosa COX-2 mRNA.