“…Some studies reported that baicalin directly reduced arachidonic acid metabolism via inhibition of phospholipase A2 (PLA2), COX and 5-lipoxygenase (5-LOX), leading to a decrease in the production of leukotrienes (LTs), thromboxanes (TXB), and prostaglandins (PGs) as well as the infiltration of inflammatory cells and MPO release in chronic inflammatory response [11,[30][31][32][33]. Furthermore, baicalin inhibited the pro-inflammatory gene expression via down-regulating the TLRs/NF-κB signaling, such as COX-2, iNOS, TNF-α , IL-6, IL-13 and HMBG-1 in cervical tissue and colon tissue [11,30,32]. In addition, baicalin inhibited the production of IL-1β, IL-8, PGE2, leukotriene B4 (LTB4), COX-2, RANKL/OPG ratio, and inhibited the NF-κB, p38 MAPK in many types of cells involved in the process of periodontitis, such as human gingival fibroblasts, periodontal ligament cells, oral keratinocytes and cultured osteoblasts [19,20,[34][35][36].…”