SCHB exerts therapeutic effects against MDD through a multifaceted molecular mechanism: it upregulates miR-124 expression, thereby suppressing NF-κB/TLR4/Myeloid differentiation primary response 88 (MyD88) and MAPK signaling pathways, which induces microglial M1 to M2 phenotypic conversion, reduces neuroinflammation, and ultimately ameliorates depression-like behaviors (Yang et al., 2024b). This evidence concerns the gene TLR4 and major depressive disorder.