Following ischemic stroke, SAC exerts dual regulatory effects by suppressing both the activation of nuclear factor-κB (NF-κB) through inhibition of Toll-like receptor 4 (TLR4)/triggering receptor expressed on myeloid cells-1 (TREM1) signaling pathways in myeloid cells and microglial overactivation, thereby reducing the expression of proinflammatory mediators (Guo et al., 2024; Shen et al., 2022). Here, TLR4 is linked to ischemic stroke.