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机构地区:[1]航天中心医院 北京大学航天临床医学院消化科,北京100049 [2]航天中心医院 北京大学航天临床医学院老年科,北京100049 [3]北京世纪坛医院 北京大学第九临床医学院消化科
出 处:《中华医学杂志》2017年第36期2852-2855,共4页National Medical Journal of China
基 金:北京市自然科学基金(7132207)
摘 要:目的观察微小RNA-24-3p(miR-24-3p)在胃黏膜病变演化过程中的表达变化,并分析其与幽门螺杆菌(Hpylori)感染的关系。方法收集2005年9月至2012年6月航天中心医院消化科行胃镜检查的患者的石蜡包埋胃组织样本共158例,根据组织形态学检查分为4组:慢性浅表性胃炎(CSG)35例、慢性萎缩性胃炎(CAG)43例、肠上皮化生(IM)41例、异型增生(Dys)39例;用快速尿素酶试验及Warthin—Starry银染检测Hpylori感染;用原位杂交方法检测各组miR-24-3p的表达。结果miR-24-3p在CSG、CAG、IM、Dys中的表达率分别为80.0%(28/35)、39.5%(17/43)、36.6%(15/41)、38.4%(15/39),CSG组中miR-24-3p的表达率明显高于其他各组(P〈0.01)。Hpylori阳性的CSG标本中,miR-24-3p的表达率较相应Hpylori阴性标本显著降低(P=0.001),在其他各组中miR-24.3p的表达率与Hpylori感染状态无相关性(均P〉0.05)。结论miR-24—3p在胃黏膜病变演化早期阶段高表达,并随胃黏膜病变的进展而降低;Hpylori在胃黏膜病变演化的早期阶段抑制了miR-24-3p的表达。Objectives To explore the expression of micro RNA-24-3p (miR-24-3p) in different gastric mucosa lesions, and analyze the potential correlation between Helicobacter pylori ( H. pylori) infection and miR-24-3p expression in different gastric lesions. Methods 158 gastric biopsy specimens were divided into four groups, including 35 chronic superficial gastritis (CSG) samples, 43 chronic atrophic gastritis (CAG) samples, 41 intestinal metaplasia (IM) samples and 39 dysplasia (Dys) samples. Those samples were collected from patients undergoing gastroscopy at the Department of Gastroenterology, Aerospace Center Hospital, from September 2005 to June 2012. The expression of miR-24-3p was detected using in situ hybridization. H. pylori infection status was determined by rapid urease test and Warthin-Starry stain. Results Higher expression rate of miR-24-3p was observed in CSG compared with those in CAG, IM and Dys, respectively. The miR-24-3p expression rate in CSG with H. pylori infection was significantly lower than that without H. pylori infection ( P = 0. 001 ), but it was not observed in CAG, IM and Dys groups ( all P 〉 0. 05). Conclusions MiR-24-3p was highly expressed at the early stage of gastric mucosal lesion. Attenuation of miR-24-3p expression is associated with the development of severe gastric mucosa lesions. H. pylori may play a role in miR-24-3p regulation in the early stage of gastric mucosa lesions.
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