针对艾拉(5-ALA)光动力治疗(PDT)中光敏活性产物原卟啉(PPIX)易失活及乏氧等制约PDT的关键问题，将胞内离子稳态与肿瘤代谢共生理论结合，以高效装载5-ALA的壳聚糖(CA)为核，CaP为壳，制备载药纳米活性载体，并结合巨噬细胞仿生，构建双离子稳态“杠杆调控”PDT系统。该系统凭借巨噬细胞膜天然肿瘤归巢效应，高效蓄积于肿瘤。被肿瘤细胞摄取后，CaP响应溶酶体酸性环境快速降解并大量释放Ca2+，同时释放出5-ALA和CA。过载的Ca2+抑制线粒体乳酸摄入，进而抑制TCA，降低氧消耗，改善乏氧(上调Ca2+，打破Ca2+稳态)；同时，CA高效络合胞内游离Fe2+/3+，避免PPIX向血红素转化失活，增加其胞内蓄积(下调游离Fe2+/3+，打破Fe2+/3+稳态)。该系统对肿瘤细胞双离子稳态“杠杆调控”同时改善影响5-ALA的 PDT效率限制因素：光敏活性产物及氧含量，协同增强PDT。

Aiming at the key problems of photosensitive active product protoporphyrin (PPIX) inactivation and hypoxia, which restricting PDT in the photodynamic therapy (PDT) of Aila (5-ALA), a bi-ionic stable "lever-controlled" PDT system is constructed by combining intracellular ion homeostasis with the symbiosis theory of tumor metabolism, using chitosan (CA) loaded with 5-ALA as the core and CaP as the shell. By virtue of the natural tumor homing effect of macrophage membrane, the system can effectively accumulate in tumors. Upon uptake by tumor cells, CaP rapidly degrades in response to the lysosomal acidic environment and releases a large amount of Ca2+ while releasing 5-ALA and CA. Overloaded Ca2+ inhibits the uptake of mitochondrial lactic acid, thereby inhibiting TCA, reducing oxygen consumption and improving hypoxia (upregulating Ca2+, breaking Ca2+ homeostasis); at the same time, CA efficiently complexes intracellular free Fe2+/3+ to avoid the inactivation of PPIX convert to heme, which increases its intracellular accumulation (downregulation of free Fe2+/3+, breaking Fe2+/3+ homeostasis). The system can regulate the bi-ionic homeostasis of tumor cells by leverage and improve the efficiency limitation factors of PDT affecting 5-ALA: photosensitive active products and oxygen content, and synergistically enhance PDT.