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Introduction
Pathological autoimmunity, which can cause conditions such as arthritis, can be treated with glucocorticoids (GCs) and nonsteroidal anti-inflammatory drugs, however their use is often limited by the adverse effects they can cause and novel anti-inflammatory therapies are required (1,2). Traditional herbal medicine has been widely used for treating various inflammatory diseases in Eastern Asia (3,4). Yunnan Baiyao (YNB) is a widely used traditional Chinese herbal remedy, and has since been used to treat various conditions, including bleeding (5), ulcers (6), infection (7), hemangiosarcoma (8) and inflammatory bowel disease (9).
Liu et al (10) reported that YNB could reduce ulcer size and accelerate healing in aphthous stomatitis. In a mouse model of colitis, Li et al (9) also established that the immunosuppressive activity of YNB involved highly selective cytotoxicity towards B and T lymphocytes, and inhibition of tumor necrosis factor α and interferon γ expression in the colonic mucosa and plasma. In a previous study, it was identified that YNB could reduce symptoms of rheumatoid arthritis in a mouse model (11). YNB-induced amelioration of foot paw swelling and inflammation was identified to be associated with reduced plasma levels of prostaglandin (PG) E2 (PGE2) and interleukin 1β, and plasma metabolomics analysis indicated that changes in circulating levels of arachidonic acid (AA) were recovered as a result of YNB administration (11).
The phospholipase A2 (PLA2)/AA pathway is a pivotal regulator of inflammatory responses. AA, liberated from the membrane phospholipids by PLA2, acts as a substrate for cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX) to produce eicosanoids, including PGs and leukotrienes (LTs); important inflammatory mediators responsible for characteristic symptoms of inflammation. COX-2, is an inducible enzyme, which is mainly expressed under pathological conditions such as inflammation. Activation of the COX-2 pathway causes PG production. 5-LOX is a major isozyme component of the LOX pathway, which catalyzes biosynthesis of LTs from AA (12). Hence, inhibition of COXs and LOX can modulate AA metabolism and inhibit inflammation. Cytosolic PLA2 (cPLA2) serves an important role in liberation of AA from membrane phospholipids (13,14). Once AA is released, it is metabolized by COXs and 5-LOX pathways (15). The AA pathway generates potent inflammatory mediators: PGs and LTs (16). COX2 catalyzes the two step conversion of AA to PGH2. This transformation begins with formation of...