The exposure of macrophage cells to bacterial LPS is well known to increase iNOS gene expression and excessive production of NO for prolonged periods, leading to the initiation of an inflammatory response. This excessive production of NO also attacks normal tissue surrounding the infected area by binding with other superoxide radical and act as a reactive radical which damages normal cell function ( Korhonen et al., 2005, Min et al., 2009 and Tewtrakul et al., 2009). Therefore, the inhibition of NO production may be beneficial in therapeutic consideration of inflammatory disorders.