CAJ | 학술논문

目的通过检测幽门螺杆菌(Hp)感染及根除治疗对慢性胃炎和胃溃疡组织中巨噬细胞移动抑制因子(MIF)蛋白表达的影响,探讨MIF和Hp在慢性胃炎和胃溃疡发生发展中的作用.方法胃镜下随机采集胃黏膜活检组织,经14C呼气试验、Warthin-starry银染色法检测Hp均为阳性,并经病理检验证实为浅表性胃炎、萎缩性胃炎、胃溃疡各40例,Hp阴性的健康检查者25例,采用免疫组织化学SP方法分别检测各组MIF蛋白的表达;进行Hp根治治疗2周,停药4周后复查Hp及MIF,比较根除前后各组MIF水平.结果 MIF蛋白在Hp阴性的正常胃黏膜中阳性表达低(2/25,8%);在Hp感染的慢性浅表性胃炎(12/40,30%)、萎缩性胃炎(26/40,65%)和胃溃疡组织(19/40,47.5%)阳性表达增强,显著高于Hp阴性的正常胃黏膜组(57/120 vs. 2/25;χ~2=13.376,P<0.01);在慢性炎症中,随着炎症程度增加,MIF表达增强,差异有显著性(12/40 vs. 26/40;χ~2=9.825,P<0.01);Hp根除后,MIF蛋白表达阳性率较治疗前显著降低(57/120 vs. 23/103;χ~2=15.264, P<0.01),而Hp仍为阳性者MIF蛋白阳性率无显著变化.结论 Hp感染导致的胃黏膜慢性炎症及溃疡的形成与胃黏膜MIF的表达相关,根除Hp感染可降低胃黏膜MIF基因表达的异常,可能对预防或减缓胃癌的发生和发展具有重要意义.
목적 통과검측유문라간균(Hp)감염급근제치료대만성위염화위궤양조직중거서세포이동억제인자(MIF)단백표체적영향,탐토MIF화Hp재만성위염화위궤양발생발전중적작용.방법 위경하수궤채집위점막활검조직,경14C호기시험、Warthin-starry은염색법검측Hp균위양성,병경병리검험증실위천표성위염、위축성위염、위궤양각40례,Hp음성적건강검사자25례,채용면역조직화학SP방법분별검측각조MIF단백적표체;진행Hp근치치료2주,정약4주후복사Hp급MIF,비교근제전후각조MIF수평.결과 MIF단백재Hp음성적정상위점막중양성표체저(2/25,8%);재Hp감염적만성천표성위염(12/40,30%)、위축성위염(26/40,65%)화위궤양조직(19/40,47.5%)양성표체증강,현저고우Hp음성적정상위점막조(57/120 vs. 2/25;χ~2=13.376,P<0.01);재만성염증중,수착염증정도증가,MIF표체증강,차이유현저성(12/40 vs. 26/40;χ~2=9.825,P<0.01);Hp근제후,MIF단백표체양성솔교치료전현저강저(57/120 vs. 23/103;χ~2=15.264, P<0.01),이Hp잉위양성자MIF단백양성솔무현저변화.결론 Hp감염도치적위점막만성염증급궤양적형성여위점막MIF적표체상관,근제Hp감염가강저위점막MIF기인표체적이상,가능대예방혹감완위암적발생화발전구유중요의의.
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 Warthin-starry method. We recruited 25 healthy people with normal gastric mucosa, 40 patients pathologically confirmed Hp-positive 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 Hp-infected chronic superficial gastritis, atrophic gastritis and gastric ulcer for 2 weeks. Hp and MIF were re-examined 4 weeks after drug withdrawal, and difference in MIF expression was compared between Hp-infected patients and Hp-eradicated patients. Results The expression of MIF was low in normal gastric mucosa without Hp infection (2/25, 8%), but significantly higher in Hp-infected 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 comHp-infected patients (57/120 vs. 2/25; χ~2=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; χ~2=9.825, P<0.01). The expression of MIF was noticeably decreased after Hp eradication compared with before(57/120 vs. 23/103; χ~2=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.