Biol. Pharm. Bull. 30(1) 59—62 (2007)

lation of a series of enzymes and signaling proteins in affected tissues and cells. Among the proinflammatory enzymes, the inducible forms of nitric oxide synthase (NOS) and cyclooxygenase (COX), which are responsible for increasing the levels of nitric oxide (NO) and prostaglandins (PGE2), are known to be involved in various chronic diseases including multiple sclerosis, Parkinson’s and Alzheimer’s diseases, and colon cancer. Lipopolysaccharide (LPS), which is a component of the cell wall of gram-negative bacteria, is known to activate a number of cellular signals of human monocytic cells during inflammation and infection. NO is synthesized by many cell types involved in immune and inflammatory response. In the THP-1 cells, inducible NOS (iNOS) triggered the production of NO after LPS-stimulation. Cyclooxygenase (COX) is a key enzyme in regulating the formation of PGE2 from arachidonic acid. There are two isoforms of cyclooxygenase, namely cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). COX-1 is in a constitutively expressed form in normal physiologic functions, whereas COX-2 is expressed only in response to inflammatory signals such as cytokines and bacterial endotoxin LPS. COX-2 is responsible for the elevated production of PGE2 during inflammation. 6) After lactoferrin and b-amyloid treatment, transcription of most genes for inflammatory proteins such as TNF-a , IL-4, IL-6, and IL-8 was inhibited in LPS-induced human monocytic cells. Tetrandrine (TET), a bis-benzylisoquinoline alkaloid, is isolated from the roots of Stephania tetrandrae S. MOORE. It is traditionally used in China for treating patients with arthritis, arrhythmia, hypertension, inflammation and silicosis. Previous reports indicated that TET possesses anticancer, immunosuppressive, and free radical scavenging activities. Although its mechanism of anti-inflammation remains unclear, TET has been shown to exhibit anti-inflammatory effect on mouse ear edema. In this study, our aim was to investigate the anti-inflammatory mechanism of TET through measuring the inducible nitric oxide synthase (iNOS), cyclooxygenase-1 and -2 (COX-1 and COX-2) expression, cytokines (TNF-a , IL-4 and IL-8) formation, nitric oxide (NO) release and prostaglandin E2 (PGE2) generation in lipopolysaccharide (LPS)-induced THP-1 cells.