以脂质代谢重编程与氧化应激为核心:中药单体成分、提取物及复方干预非小细胞肺癌分子机制研究进展OA

Non-small cell lung cancer(NSCLC)is one of the malignancies with the highest mortality worldwide.Despite significant advances in targeted therapy and immunotherapy,acquired drug resistance and adverse effects remain major clinical bottlenecks.Evidence indicates that the interactive network between lipid metabolic reprogramming and oxidative stress homeostasis imbalance constitutes an intrinsic mechanism driving malignant progression and therapeutic resistance in NSCLC.Studies have shown that NSCLC cells exhibit metabolic characteristics marked by a surge in de no-vo lipid synthesis and a state of high-level reactive oxygen species(ROS)accompanied by enhanced antioxidant capaci-ty.Evidence suggests that Fuzheng(扶正)agents,represented by ginsenosides and astragaloside IV,can inhibit the PI3K/Akt/mTOR pathway and activate AMPK,thereby downregulating the SREBP-1/FASN/ACC axis and blocking lip-id synthesis at its source.In contrast,Quxie(祛邪)agents,represented by artemisinin,shikonin,and cinobufotalin,dis-rupt redox homeostasis and induce ferroptosis by promoting iron-dependent ROS generation,inhibiting the Nrf2 antioxi-dant pathway,and accelerating GPX4 degradation.Such remodeling of the"lipid metabolism-oxidative stress"network ultimately translates into multidimensional pharmacological effects,including inhibition of proliferation,induction of pro-grammed cell death,reversal of drug resistance,and improvement of the immune microenvironment.This review aims to systematically elucidate the molecular mechanisms underlying the multi-target,network-based intervention of Chinese medicine in NSCLC,using the"lipid metabolism-oxidative stress"axis as the central pathological entry point.