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作 者:李慕琦[1] 余保平[1] 胡国勇[1] 罗和生[1] 于皆平[1] 冉宗学[1]
机构地区:[1]武汉大学人民医院消化内科,湖北省武汉市430060
出 处:《世界华人消化杂志》2003年第1期39-42,共4页World Chinese Journal of Digestology
摘 要:目的:观察三叶肽因子2(trefoilpeptide2,TFF2)在胃癌及癌前病变中的表达状况及其与Hp感染的关系,初步探讨TFF2与Hp感染在胃癌及癌前病变中的作用及意义.方法:应用免疫组化方法测定16例慢性浅表性胃炎,20例慢性萎缩性胃炎,35例肠上皮化生,23例胃上皮不典型增生和25例胃癌中TFF2的蛋白表达情况,同时应用Warthin-Starry法检测幽门Hp情况.结果:(1)在慢性浅表性胃炎,慢性萎缩性胃炎,胃上皮不典型增生中均有TFF2的阳性表达,其阳性率分别为100%,100%和56.5%.而在肠上皮化生和胃癌组织内无TFF2的阳性表达,但在肠上皮化生周围的正常腺体有TFF2阳性表达.慢性浅表性胃炎TFF2的染色评分明显高于慢性萎缩性胃炎组.(2)在浅表性胃炎中,Hp感染阳性病例TFF2的阳性细胞密度值高于Hp感染阴性者(52.9±7.3vs46.5±13.0),但无统计学意义(P>0.05).而在胃黏膜萎缩及胃黏膜上皮不典型增生中,Hp感染者TFF2的阳性细胞密度值又低于Hp感染阴性者,差异有显著性(18.2±4.1vs37.9±13.8,P<0.01和14.4±9.3vs24.8±10.2,P<0.05).结论:TFF2在慢性浅表性胃炎中的高表达与黏膜损伤后所诱导的保护机制有关;慢性萎缩性胃炎TFF2的表达相对减少可能与分泌TFF2的胃黏膜腺体减少有关;但在不典型增生中TFF2的再表达可能参与了胃癌发生的早期阶段;Hp感染对TFF2表达的影响可能取决于胃黏膜病变的状态.AIM:To investigate the relationship between the expres- sion of TFF2 and H.pylori infection in human gastric precan- cerous lesions and gastric cancer, and to explore the role of TFF2 and H.pylori in human gastric precancerous lesions and gastric cancer. METHODS:The expression of TFF2 was immunohistochemic- ally analyzed in paraffin-embedded samples obtained by endoscopic biopsy and subtotal gastractomy specimens from 119 patients including chronic superficial gastritis (CSG, 16), chronic atrophic gastritis (CAG, 16), intestinal metaplasia (IM, 35), gastric epithelial dysplasia (GED, 23) and gastric cancer (CA, 25), and conditions of H.pylori infection were detected by means of Warthin-Starry staining. RESULTS:TFF2 was located in the cell plasma of gastric mucous neck cells. The expressions of TFF2 were 100 %, 100 %, 0%, 56 % and 0% in CSG, CAG, IM, GED and CA, respectively. The density of TFF2 positive cells was higher in CSG with H.pylori infection than that without H. pylori infection (52.9±7.3 vs 46.5±13.0, P >0.05); but it was sig- nificantly lower in CAG and GED with H. pylori infection than that without H. pylori infection (18.2±4.1 vs 37.9±13.8, P <0.01 and 14.4±9.3 vs 24.8±10.2, P <0.05). CONCLUSION:The high expression of TFF2 is associated with the protective mechanism after the gastric mucosal injury, the low expression of TFF2 in CAG might attribute to the decreased number of gastric gland cells secreting TFF2; but the re-expression of TFF2 in GED suggests that TFF2 is involved with the initiation of gastric cancer. The effect ofH. pylori on the expression of TFF2 depends on the status of gastric mucosa.
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