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基于cag致病岛探讨胃"炎-癌"转化的中医核心病机

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幽门螺杆菌(Helicobacter pylori,HP)是目前已知的诱发胃癌的首要可控危险因素。cag致病岛作为Ⅰ型HP强致病力产毒菌株的特殊生理学标志,具有编码致病菌中毒素、黏附因子、侵袭因子或其他毒力因子基因的作用,与HP对胃上皮细胞的毒力损害和致癌机制有直接关系。结合现代医学cag致病岛诱导胃"炎-癌"转化机制与中医学理论研究,认为胃"炎-癌"转化的中医核心病机为"脾虚湿困,毒损络阻"。本文通过探讨cag致病岛及其相关毒力因子的致炎致癌机制,阐释胃"炎-癌"转化的中医核心病机及诊治规律,以求探索有益于延缓、逆转胃"炎-癌"转化级联过程的中西医结合诊疗思路。
Explore the core pathogenesis of gastric"inflammation-cancer"transformation based on cag pathogenic island
Helicobacter pylori(HP)is a well-established controllable risk factor for gastric cancer.The HP pathogenic island serves as a distinctive physiological marker for type Ⅰ HP strains that are strong producers of pathogenic viruses.It contains genes encoding toxins,adhesion factors,invasion factors,and other virulence fac-tors,which are directly linked to the pathogenic damage and carcinogenic mechanisms of HP on epithelial cells.This paper integrates modern medical research on the"inflammation-cancer"transformation mechanism in the stomach with the theoretical study of Traditional Chinese Medicine(TCM).It posits that the core pathogenesis of TCM in gastric"inflammation-cancer"transformation is characterized by"spleen deficiency,dampness and turbid-ity,and toxic damage with collateral obstruction".The paper discusses the carcinogenic mechanisms of the cag pathogenic island and its associated virulence factors,elucidates the core pathogenesis of TCM,and outlines the diagnostic and treatment principles for gastric"inflammation-cancer"transformation.The aim is to explore diag-nostic and treatment concepts that combine TCM with Western medicine,which could be beneficial in delaying and reversing the cascade process of gastric"inflammation-cancer"transformation.

cag pathogenic islandHelicobacter pylorigastric"inflammation-cancer"transformationgas-tric cancerpathogenesis

姜天童、刘震、白宇宁、王少丽、田志华、陈敬予、李萌

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中国中医科学院广安门医院消化科(北京,100053)

cag致病岛 幽门螺杆菌 胃"炎-癌"转化 胃癌 病机

国家自然科学基金资助项目国家中医药多学科交叉创新团队项目

82174352ZYYCXTD-D-202205

2024

中国中西医结合消化杂志
华中科技大学同济医学院,中国中西医结合学会消化系统疾病专业委员会,中华中医药学会脾胃病专业委员会

中国中西医结合消化杂志

CSTPCD
影响因子:1.363
ISSN:1671-038X
年,卷(期):2024.32(8)