ITGAM and Sepsis: Li et al. reported that emodin significantly inhibited degranulation of mast cells induced by LPS and reduced expression of L-selectin, intercellular adhesion molecule 1 (ICAM-1), CD11b, activator protein-1 (AP-1), toll-like receptor 4 (TLR4), and nuclear factor kappa B p65 (NF-κB p65), suggesting emodin's beneficial role in ameliorating microcirculatory disturbance (adhesion molecule expression, leukocyte adhesion, and cytokine release) by a possible pathway involving TLR4, NF-κB, and AP-1 in sepsis animals [34].