The anti-inflammatory effects of Yunnan Baiyao are involved in regulation of the phospholipase A2/arachidonic acid metabolites pathways in acute inflammation rat model.

The traditional Chinese medicine Yunnan Baiyao (YNB) has been reported to possess anti­inflammatory properties, however its mechanism of action remains unclear. It was previously reported that YNB ameliorated depression of arachidonic acid (AA) levels in a rat model of collagen-induced arthritis. In the current study, the capacity of YNB to ameliorate inflammation was compared in carrageenan­induced and AA­induced acute inflammation of the rat paw with celecoxib and mizolastine, respectively (n=24 per group). The capacity of YNB to affect the phospholipase A2 (PLA2)/AA pathway (using reverse transcription­quantitative polymerase chain reaction) and release of inflammatory lipid mediators (by ELISA) were investigated. Celecoxib ameliorated carrageenan­induced paw edema, and mizolastine ameliorated AA­induced rat paw edema. YNB alleviated paw edema and inhibited inflammatory cell infiltration in the two models. YNB inhibited production of 5­LOX AA metabolite leukotriene B4 (LTB4), and suppressed expression of 5­LOX, cytosolic PLA2 (cPLA2), 5­LOX­activating protein, and LTB4 receptor mRNA in the AA­induced inflammation model (P<0.05). YNB Inhibited the production of the COX­2 AA metabolite prostaglandin E2 (PGE2) and suppressed expression of COX­2, cPLA2, PGE2 mRNA in the carrageenan­induced inflammation mode (P<0.05). Taken together, the data suggest that modulation of COX and LOX pathways in AA metabolism represent a novel anti-inflammatory mechanism of YNB.