| 张茜，王俊莹，葛惠男，沈贤敏，龚诚，刘敏.胃癌前病变中有氧糖酵解的作用机制及中医药干预研究进展[J].中医药信息,2026,43(6):83-90 |
| 胃癌前病变中有氧糖酵解的作用机制及中医药干预研究进展 |
| Research Progress on the Mechanism of Aerobic Glycolysis in Gastric Precancerous Lesions and Intervention with Traditional Chinese Medicine |
| 投稿时间：2025-11-21 录用日期：2026-01-01 |
| DOI：10.19656/j.cnki.1002-2406.20260613 |
| 中文关键词: 胃癌前病变 有氧糖酵解 瓦博格效应 中医药 |
| 英文关键词: Gastric precancerous lesions Aerobic glycolysis Warburg effect Traditional Chinese medicine |
| 基金项目:江苏省名老中医药传承工作室建设项目（苏中医科教[2019]10号）；苏州市科技发展计划项目（SYSD2019243） |
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| 中文摘要: |
| 胃癌前病变是胃癌发生的关键可逆阶段，其恶性进展与有氧糖酵解的异常活化密切相关。有氧糖酵解通过调控关键代谢酶及上游信号通路驱动乳酸生成与酸性微环境形成，从而促进胃癌前病变进展。中医药具有“整体调节、多靶点干预”的优势，在调控有氧糖酵解、逆转胃癌前病变中展现出良好潜力。本文系统综述了有氧糖酵解在胃癌前病变中的分子机制及中医药干预进展，发现中药单体及复方可协同调控多环节，通过多靶点调控糖酵解关键酶（如葡萄糖转运蛋白1、己糖激酶2、丙酮酸激酶M2、乳酸脱氢酶A）及上游信号通路［如缺氧诱导因子－1α、磷脂酰肌醇3－激酶（PI3K）/蛋白激酶B（Akt）/雷帕霉素靶蛋白（mTOR）通路］，有效抑制乳酸蓄积与酸性微环境形成，进而逆转病变进程，其作用机制与中医“脾虚、血瘀、毒损”病机相契合，体现了传统辨治与现代代谢调控机制的科学结合。 |
| 英文摘要: |
| Gastric precancerous lesions are a key reversible stage in gastric carcinogenesis， and their progression is closely associated with the aberrant activation of aerobic glycolysis. Aerobic glycolysis drives the generation of lactic acid and the formation of an acidic microenvironment by regulating key metabolic enzymes and upstream signaling pathways， thereby promoting the progression of gastric precancerous lesions. Traditional Chinese medicine （TCM）， with its advantages of "holistic regulation and multi－target intervention"， has shown great potential in regulating aerobic glycolysis and reversing gastric precancerous lesions. This study systematically reviews the molecular mechanisms of aerobic glycolysis in gastric precancerous lesions and the progress of TCM intervention. It is found that TCM monomers and compound formulas can synergistically regulate multiple aspects of the process. They can effectively inhibit the accumulation of lactic acid and the formation of an acidic microenvironment by multi－target regulation of key glycolytic enzymes （such as glucose transporter 1， hexokinase 2， pyruvate kinase M2， and lactate dehydrogenase A） and upstream signaling pathways ［such as hypoxia－inducible factor－1α and phosphatidylinositol 3－kinase （PI3K）/protein kinase B （Akt）/mammalian target of rapamycin （mTOR）］， thereby reversing the lesion process. Their mechanisms of action are consistent with the pathogenesis of "spleen deficiency， blood stasis， and toxic damage" in TCM， demonstrating the scientific combination of traditional syndrome－based treatment and modern metabolic regulation mechanisms. |
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