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从胆汁酸与肠上皮化生和胃内微生物(幽门螺杆菌和非幽门螺杆菌)的关系探讨胃癌的发生机制。

Exploration of gastric carcinogenesis from the relationship between bile acids and intestinal metaplasia and intragastric microorganisms (H. pylori and non-H. pylori).

机构信息

Department of Gastroenterology, The Lanzhou University Second Hospital, No. 82 of Linxia Street, Chengguan District, Lanzhou, 730030, China.

出版信息

J Cancer Res Clin Oncol. 2023 Dec;149(18):16947-16956. doi: 10.1007/s00432-023-05407-5. Epub 2023 Sep 14.

DOI:10.1007/s00432-023-05407-5
PMID:37707577
Abstract

Gastric cancer (GC) is a prevalent form of cancer, with Helicobacter pylori (H. pylori) infection being the most common risk factor. Recent studies have highlighted the role of long-term irritation of the gastric mucosa caused by bile reflux in the development of cancer. Bile acids (BAs), which are a significant component in bile reflux, have the potential to promote gastric carcinogenesis through various mechanisms. These mechanisms include the induction of intestinal metaplasia (IM), inhibition of H. pylori activity, modification of H. pylori colonization, and alteration of the abundance and composition of microorganisms in the stomach. Defining the mechanism of bile acid-induced gastric carcinogenesis could potentially be an effective approach to prevent GC. Hence, this paper aims to review the mechanism of bile acid-induced IM, the association between BAs and H. pylori infection as well as microorganisms in the stomach, and the correlation between BAs and gastric carcinogenesis. The ultimate goal is to elucidate the role of BAs in the development of GC.

摘要

胃癌(GC)是一种常见的癌症,其中幽门螺杆菌(H. pylori)感染是最常见的危险因素。最近的研究强调了胆汁反流对胃黏膜的长期刺激在癌症发展中的作用。胆汁酸(BAs)是胆汁反流的重要组成部分,通过多种机制可能促进胃癌的发生。这些机制包括诱导肠上皮化生(IM)、抑制 H. pylori 活性、改变 H. pylori 定植、以及改变胃内微生物的丰度和组成。确定胆汁酸诱导胃癌发生的机制可能是预防 GC 的有效方法。因此,本文旨在综述胆汁酸诱导 IM 的机制、BAs 与胃内 H. pylori 感染和微生物的关系,以及 BAs 与胃癌发生的相关性。最终目的是阐明 BAs 在 GC 发展中的作用。

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Int J Mol Sci. 2023 Aug 26;24(17):13268. doi: 10.3390/ijms241713268.
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Alteration of gastric microbiota and transcriptome in a rat with gastric intestinal metaplasia induced by deoxycholic acid.
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