目的 評(píng)估阿魏酸對(duì)幽門螺桿菌Helicobacter pylori致胃炎小鼠Wnt/β連環(huán)蛋白（β-catenin）信號(hào)轉(zhuǎn)導(dǎo)通路的影響。方法 采用H.pylori和N-甲基-N'-硝基-N-亞硝基胍（MNNG）聯(lián)合誘導(dǎo)法制備C57BL/6小鼠胃炎模型，分為模型組、鉍劑四聯(lián)（陽性藥）和阿魏酸高、低劑量（100、50 mg·kg^-1）組，另設(shè)對(duì)照組。ig給藥4周后，通過尿素酶試驗(yàn)評(píng)價(jià)H.pylori的定植程度；通過ELISA試驗(yàn)檢測腫瘤壞死因子α（TNF-α）、白細(xì)胞介素8（IL-8）的血清水平；通過免疫組化試驗(yàn)檢測胃黏膜Wnt2、β-catenin的蛋白表達(dá)。結(jié)果 模型組H.pylori定植率100%，阿魏酸高、低劑量組H.pylori清除率顯著增加為67%、64%（P＜0.01）；與模型組比較，阿魏酸高、低劑量可使胃炎動(dòng)物血清TNF-α、IL-8水平顯著降低（P＜0.01），可明顯下調(diào)胃黏膜中Wnt2、β-catenin的蛋白表達(dá)（P＜0.01）。結(jié)論 阿魏酸具有減輕H.pylori定植程度、減輕胃黏膜炎癥反應(yīng)等作用，其作用機(jī)制與抑制Wnt/β-catenin信號(hào)通路的異?；罨⑾抡{(diào)炎癥因子的高表達(dá)等有關(guān)。

Objective To evaluate the effect of ferulic acid (FA) on the Wnt/β -catenin signal pathway in mice with Helicobacter pylori-induced gastritis. Methods Gastritis model in C57BL/6 mice was prepared by a combination of H. pylori infection and MNNG inducement. Then mice with gastritis were divided at random into model group, FA high and low dose groups and positive group (bismuth potassium citrate + omeprazole + clarithromycin + amoxicillin). The normal group of mice was set up at the same time. After four weeks of oral administration of medicines, the H. pylori colonization in mice were evaluated by rapid urase test. The ELISA experiments were carried out to measure the TNF- α and IL-8 levels in sera of mice. The protein expression of Wnt2 and β-catenin in gastric mucosa were determined by immunohistochemical test. Results The H. pylori colonization rate was 100% in the model group. Comparing with that of model group, H. pylori eradication rates in groups treated with high and low doses of FA were evidently increased to 67% and 64%, respectively (P＜0.01). FA (100 and 50 mg·kg-1) evidently decreased the serum TNF-α and IL-8 contents of the gastritis animals, and the differences were statistically significant when compared with those of the model group (P＜0.01). High and low doses of FA significantly reduced the protein expression of Wnt2 and β-catenin in gastric mucosa of mice with gastritis comparing with those of model group (P＜0.01). Conclusion FA could alleviate the degree of H. pylori colonization, relieve the inflammatory reaction and prevent the epithelial-mesenchymal transition, showing a protective effect on gastric mucosa in mice with H. pylori-induced gastritis. The prevention of abnormal activation of Wnt/β-catenin signal pathway and inhibition of inflammatory cytokines expression may explain the mechanisms of FA in treating gastritis.

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河南省高?？萍紕?chuàng)新人才支持計(jì)劃項(xiàng)目（編號(hào)15HASTIT041）