 |
 |
醫(yī)學(xué)論文范文:根除幽門螺桿菌對慢性胃炎和胃潰瘍組織中MIF蛋白表達(dá)的影響
【摘要】 目的 通過檢測幽門螺桿菌(Hp)感染及根除治療對慢性胃炎和胃潰瘍組織中巨噬細(xì)胞移動(dòng)抑制因子(MIF)蛋白表達(dá)的影響，探討MIF和Hp在慢性胃炎和胃潰瘍發(fā)生發(fā)展中的作用。方法 胃鏡下隨機(jī)采集胃黏膜活檢組織，經(jīng)14C呼氣試驗(yàn)、Warthinstarry銀染色法檢測Hp均為陽性，并經(jīng)病理檢驗(yàn)證實(shí)為淺表性胃炎、萎縮性胃炎、胃潰瘍各40例，Hp陰性的健康檢查者25例，采用免疫組織化學(xué)SP方法分別檢測各組MIF蛋白的表達(dá);進(jìn)行Hp根治治療2周，停藥4周后復(fù)查Hp及MIF，比較根除前后各組MIF水平。結(jié)果 MIF蛋白在Hp陰性的正常胃黏膜中陽性表達(dá)低(2/25，8%);在Hp感染的慢性淺表性胃炎(12/40，30%)、萎縮性胃炎(26/40，65%)和胃潰瘍組織(19/40，47.5%)陽性表達(dá)增強(qiáng)，顯著高于Hp陰性的正常胃黏膜組(57/120 vs. 2/25;χ2=13.376，P<0.01);在慢性炎癥中，隨著炎癥程度增加，MIF表達(dá)增強(qiáng)，差異有顯著性(12/40 vs. 26/40;χ2=9.825，P<0.01);Hp根除后，MIF蛋白表達(dá)陽性率較治療前顯著降低(57/120 vs. 23/103;χ2=15.264, P<0.01)，而Hp仍為陽性者M(jìn)IF蛋白陽性率無顯著變化。結(jié)論 Hp感染導(dǎo)致的胃黏膜慢性炎癥及潰瘍的形成與胃黏膜MIF的表達(dá)相關(guān)，根除Hp感染可降低胃黏膜MIF基因表達(dá)的異常，可能對預(yù)防或減緩胃癌的發(fā)生和發(fā)展具有重要意義。
【關(guān)鍵詞】 巨噬細(xì)胞移動(dòng)抑制因子;幽門螺桿菌;慢性胃炎;胃潰瘍
Effect of Helicobacter pylori infection on macrophage migration inhibitory factor protein expression in patients withchronic gastritis and gastric ulcer precancerous lesions
ZHANG Shuangxia, LI Guangdi, YU Xiaohui, ZHANG Fangxin
1. the Second Clinical Medical College of Lanzhou University, Lanzhou 730000;2. Department of Laboratory, the Second Affiliated Hospital of Lanzhou University, Lanzhou 730000; 3. Department of Gastroenterology,Lanzhou General Hospital of Lanzhou Command, Lanzhou 730000, China醫(yī).學(xué)全.在.線52667788.cn
ABSTRACT: Objective To investigate the effect of Helicobacter pylori (Hp) infection on macrophage migration inhibitory factor (MIF) protein expression and explore the role of Hp and MIF in the development of chronic gastritis and gastric ulcer. Methods The biopsy tissues of gastric mucosa were collected under gastroscope, and Hp was detected by 14C breath test and Warthinstarry method. We recruited 25 healthy people with normal gastric mucosa, 40 patients pathologically confirmed Hppositive with chronic superficial gastritis, 40 with atrophic gastritis and 40 with gastric ulcer. MIF protein expression was examined by immunohistochemical SP staining method, then Hp eradication was performed on Hpinfected chronic superficial gastritis, atrophic gastritis and gastric ulcer for 2 weeks. Hp and MIF were reexamined 4 weeks after drug withdrawal, and difference in MIF expression was compared between Hpinfected patients and Hperadicated patients. Results The expression of MIF was low in normal gastric mucosa without Hp infection (2/25, 8%), but significantly higher in Hpinfected gastric mucosa with chronic superficial gastritis (12/40, 30%), atrophic gastritis (26/40, 65%) and gastric ulcer (19/40, 47.5%); there was a significant difference between normal gastric mucosa without Hp infection and that of Hpinfected patients (57/120 vs. 2/25; χ2=13.376, P<0.01). MIF expression increased with the severity of inflammation in chronic gastritis, and there was a significant difference between superficial gastritis and atrophic gastritis (12/40 vs. 26/40; χ2=9.825, P<0.01). The expression of MIF was noticeably decreased after Hp eradication compared with before(57/120 vs. 23/103; χ2=15.264, P<0.01); however, there was no significant change in those patients whose Hp was still positive. Conclusion The expression of MIF on gastric mucosa is associated with the development of chronic gastritis and gastritis ulcer caused by Hp infection. Eradication of Hp could cut down the abnormally high MIF expression in gastric mucosa and slow down the formation and development of gastric carcinoma.
KEY WORDS: macrophage migration inhibitory factor; Helicobacter pylori; chronic gastritis; gastric ulcer
巨噬細(xì)胞移動(dòng)抑制因子(macrophage migration inhibitory factor, MIF)是重要的炎癥因子，能抑制巨噬細(xì)胞遷移，促進(jìn)IV型過敏反應(yīng)中巨噬細(xì)胞的聚積。近年來，許多研究證明MIF參與細(xì)胞增殖和分化的調(diào)節(jié)，在多種炎癥性疾病和惡性腫瘤細(xì)胞中高表達(dá)，在胃癌中的表達(dá)顯著增高[12]，幽門螺桿菌(helicobacter pylori, Hp)是慢性胃炎、消化性潰瘍、胃癌和胃B細(xì)胞淋巴瘤重要的危險(xiǎn)因子[3]。為進(jìn)一步探討Hp和MIF在慢性胃炎胃潰瘍向胃癌發(fā)生過程中的作用，我們檢測了Hp感染的慢性淺表性胃炎、萎縮性胃炎和胃潰瘍組織中MIF的表達(dá)，并給予Hp根除治療，分析Hp根除前后MIF表達(dá)的變化，探討MIF和Hp在慢性胃炎和胃潰瘍發(fā)生發(fā)展過程中的可能作用及兩者的相關(guān)性。
