In addition, emodin can bind to c-Jun N-terminal kinase (JNK2), inhibit the activation of NF-κB signaling [35], induce a protective effect against sepsis-associated intestinal mucosal barrier injury, increase the expression of tyrosine kinase receptor B (TrkB) and brain-derived neurotrophic factor (BDNF), and significantly inhibit the inflammatory response in CLP mice, thereby improving cognitive impairment and reducing pathological damage [36]. Here, NTRK2 is linked to Sepsis.