Cavidine　is　an　isoquinoline　alkaloid　which　is　isolated　from　Corydalis　impatiens.　In　traditional　Tibetan　herb,　C.　impatiens　has　been　widely　used　for　treatment　of　skin　injuries,　hepatitis,　cholecystitis,　and　scabies.　The　present　study　aimed　to　evaluate　its　anti-inflammatory　effect　and　investigate　the　mechanisms　underlying　this　anti-inflammatory　action.　We　used　different　inflammation　model　animals　and　lipopolysaccharide　(LPS)-induced　murine　peritoneal　macrophages　to　examine　the　anti-inflammatory　function　of　cavidine.　Results　indicated　pretreatment　with　cavidine　(i.p.)　decreased　xylene-induced　ear　edema,　formaldehyde-induced　paw　edema,　leukocyte　number,　and　the　level　of　nitric　oxide　(NO),　prostaglandin　E-2　(PGE(2)),　and　tumor　necrosis　factor-alpha　(TNF-alpha)　in　acetic　acid-induced　peritonitis　in　mice.　The　data　also　demonstrated　that　cavidine　significantly　inhibited　LPS-induced　TNF-alpha,　interleukin-6　(IL-6),　and　NO　production　in　peritoneal　macrophages.　Moreover,　cavidine　regulated　the　expression　of　cyclooxygenase-2　(COX-2)　instead　of　cyclooxygenase-1　(COX-1)　at　protein　levels.　These　results　suggested　that　cavidine　is　a　selective　COX-2　inhibitor　which　possesses　an　anti-inflammatory　activity.