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基于脾虚血瘀理论探讨巨噬细胞糖代谢重编程在胃“炎癌转化”中的作用

Dicussion on the role of glucose metabolism reprogramming of macrophages in gastric inflammation-cancer transformation'based on the theory of spleen deficiency and blood stasis
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摘要 胃“炎癌转化”病机理论认为脾虚为其致病的内在因素,血瘀于脾虚基础上渐生,二者均为重要病理因素。巨噬细胞被证实为肿瘤微环境中对葡萄糖的摄取和代谢能力最强的细胞群体,可分泌炎性介质、参与炎症反应,在胃炎向胃癌转化过程中,巨噬细胞以糖代谢重编程为主发生代谢改变,重构肿瘤相关巨噬细胞表型及功能,促进“炎癌转化”,该过程与脾虚血瘀病机理论相契合。文章基于中医脾虚血瘀理论,结合胃“炎癌转化”病机和巨噬细胞糖代谢重编程与胃“炎癌转化”的相关性进行论述,以期为中医药防治胃“炎癌转化”提供参考。 The theory of gastric‘inflammation-cancer transformation'asserts that spleen deficiency is intrinsic pathogenic factors,with blood stasis stemming from spleen deficiency,which serves as a significant pathological factor in the gastric‘inflammation-cancer transformation'.Macrophages have been identified as the cell population within the tumor microenvironment with the highest capacity for glucose uptake and metabolism.They secrete inflammatory mediators and participate in the inflammatory response.During the transition from gastritis to gastric cancer,macrophages undergo metabolic changes primarily characterized by glucose metabolism reprogramming,which alters the phenotype and function of tumorassociated macrophages and promotes the‘infiammation-cancer transformation'.This process is consistent with the pathogenesis theory of‘spleen deficiency and blood stasis'.Based on the theory of‘spleen deficiency and blood stasis'in traditional Chinese medicine,this paper analyzes its correlation with macrophage glucose metabolism reprogramming and the gastric ‘infiammationcancer transformation'.This study is intended to provide a reference for the prevention and treatment of gastric‘inflammationcancer transformation'by traditional Chinese medicine.
作者 李晓方 潘华峰 LI Xiaofang;PAN Huafeng(Guangzhou University of Chinese Medicine,Guangzhou 510006,China)
机构地区 广州中医药大学
出处 《中华中医药杂志》 CAS CSCD 北大核心 2024年第9期4839-4842,共4页 China Journal of Traditional Chinese Medicine and Pharmacy
基金 广东省重点领域研发计划项目(No.2020B1111100011)。
关键词 脾虚血瘀 巨噬细胞 糖代谢重编程 胃“炎癌转化” Spleen deficiency and blood stasis Macrophages Glucose metabolism reprogramming Gastric‘inflammation-cancer transformation'
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