Prompt Description

Low concentrations of compound Af can stimulate tumor-associated macrophages (TAMs) to adopt an M1-like anti-tumor phenotype. Furthermore, the 'find me' and 'eat me' signals released by Af-induced glioblastoma multiforme (GBM) cells can further enhance the killing of GBM cells by M1-like TAMs. Af can exert toxicity on GBM cells through this TAM-dependent effect. High concentrations of Af disable TAMs and disrupt the interaction between GBM cells and TAMs, such as the positive feedback loop mediated by IL-6/STAT3, thereby eliminating its pro-GBM functions. By targeting GBM with Af-loaded platelets for Af delivery, it can synergize with chemotherapy and immunotherapy to produce anti-GBM efficacy. By loading Af together with the sonosensitizer fluorescein (Flu) onto platelets and then combining these dual-loaded platelets with directional ultrasound irradiation of GBM, Af and Flu can be targeted and actively delivered to GBM through 'ultrasound-controlled release', thereby enhancing the activity of Flu-mediated GBM sonodynamic therapy (GBM-SDT).