HERBA SAURURI (HS) has been known to use antiinflammatory drug. To investigated the mechanism of HS-induced NO synthesis, I evaluated the ability of protein kinase C (PKC) inhibitors such as staurosporine (STSN) or polyymyxin B to block HS-induced effects. HS alone had only a small effect, whereas in combination with $rIFN-{gamma}$, markedly increased NO synthesis in a dose dependent manner. STSN and polymyxin B decreased NO synthesis, which had been induced by $rIFN-{gamma}$, plus HS. Furthermore, prolonged incubation of the cells with phorbol ester, which down-regulates PKC activity abolished synergistic cooperative effect of HS with $rIFN-{gamma}$ on NO synthesis. STSN and Polymyxin B potently inhibited HS-induced $TNF-{alpha}$ secretion by $rIFN-{gamma}$ plus HS. However, $rIFN-{gamma}$ plus $TNF-{alpha}-induced$ NO synthesis was not blocked by STSN or polymyxin B. On the other hand, tyrosine kinase inhibitor, genistein, blocked the NO synthesis and $TNF-{alpha}$ secretion by $rIFN-{gamma}$ plus HS. In conlusion, the present results strongly suggest that the capacity of HS to increase NO synthesis from $rIFN-{gamma}-primed$ macrophages is the result of HS-induced $TNF-{alpha}$ secretion via the signal transduction pathway of PKC and tyrosine kinase.