1.昆明医科大学生命科学与检验医学学院,昆明 650500
2.重庆大学生物工程学院,重庆 400044
3.重庆大学附属肿瘤医院心血管内科,重庆 400030
Received:22 April 2026,
Revised:2026-10-12,
Accepted:14 October 2026,
Published:30 October 2026
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郭俊松,李莹,刘海霞,等.人参皂苷抗非小细胞肺癌作用机制的研究进展 [J].中国药房,2026,37(20):2753-2758.
GUO Junsong,LI Ying,LIU Haixia,et al.Ginsenosides against non-small cell lung cancer: advances in mechanisms of action[J].ZHONGGUO YAOFANG,2026,37(20):2753-2758.
郭俊松,李莹,刘海霞,等.人参皂苷抗非小细胞肺癌作用机制的研究进展 [J].中国药房,2026,37(20):2753-2758. DOI: 10.6039/j.issn.1001-0408.2026.20.20.
GUO Junsong,LI Ying,LIU Haixia,et al.Ginsenosides against non-small cell lung cancer: advances in mechanisms of action[J].ZHONGGUO YAOFANG,2026,37(20):2753-2758. DOI: 10.6039/j.issn.1001-0408.2026.20.20.
非小细胞肺癌(NSCLC)治疗的长期疗效受获得性耐药、复发转移及免疫抑制性肿瘤微环境的多重挑战。近年来,人参皂苷Rg
3
、Rh
2
、Rh
4
、Re及其代谢产物化合物K(CK)在NSCLC中的抗肿瘤作用逐渐受到关注。本文围绕NSCLC细胞恶性表型、肿瘤微环境与免疫应答以及联合治疗反应,梳理不同人参皂苷的作用机制。现有研究表明,人参皂苷Rg
3
可抑制细胞增殖、上皮-间质转化和血管生成
,降低程序性死亡配体1的糖基化及稳定性,并增强部分化疗、表皮生长因子受体酪氨酸激酶抑制剂和放疗方案的抗肿瘤作用;人参皂苷Rh
2
主要调控凋亡、糖酵解、肿瘤干性和肿瘤相关巨噬细胞;人参皂苷Rh
4
、Re和CK分别涉及铁死亡、内质网应激与巨噬细胞M2型极化、自噬及缺氧代谢。目前,人参皂苷Rg
3
联合化疗已有临床评价,其他单体的证据仍主要来自临床前模型。未来应在制剂标准化的基础上,结合分子特征和耐药机制开展分层研究,明确联合用药的剂量、顺序及安全性,并通过规范的前瞻性临床研究验证其作为NSCLC辅助干预的长期获益。
Long-term outcomes in non-small cell lung cancer (NSCLC) are challenged by acquired resistance, recurrence and metastasis, as well as an immunosuppressive tumor microenvironment. In recent years, the antitumor effects of ginsenosides Rg
3
, Rh
2
, Rh
4
and Re, as well as their metabolite compound K (CK), in NSCLC have attracted increasing attention. This review summarizes the mechanisms of different ginsenosides with respect to the malignant phenotypes of NSCLC cells, the tumor microenvironment and immune responses, as well as their use in combination therapy. Available evidence indicates that ginsenoside Rg
3
inhibits cell proliferation, epithelial-mesenchymal transition and angiogenesis; reduces programmed death-ligand 1 glycosylation and thereby its stability; and enhances the antitumor effects of certain chemotherapeutic agents, epidermal growth factor receptor tyrosine kinase inhibitors and radiotherapy regimens. Ginsenoside Rh
2
mainly regulates apoptosis, glycolysis and cancer stemness, and modulates tumor-associated macrophages. Ginsenoside Rh
4
is involved in ferroptosis, ginsenoside Re in endoplasmic reticulum stress and M2 macrophage polarization, and CK in autophagy and hypoxic metabolism. At present, ginsenoside Rg
3
combined with chemotherapy has been clinically evaluated, whereas evidence for the other ginsenosides is still mainly preclinical. Future studies should standardize formulations, incorporate molecular features and resistance mechanisms into stratified studies, clarify the dose, sequence and safety of combination regimens, and confirm the long-term benefits of ginsen
osides as an adjunctive intervention for NSCLC in well-designed prospective clinical trials.
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