Objective      To determine the inhibitory effect of agmatine (AGM) on lipopolysaccharides (LPS)-induced oxidative stress in mouse macrophage RAW264.7 cells and its underlying mechanism.       Methods      RAW264.7 cells were stimulated by LPS (10 μg/mL) to induce oxidative stress

and treated with 1 mmol/L AGM. Thus the cells were divided into control

LPA

LPS+AGM

and AGM groups. In 24 h after the treatment

reactive oxygen species (ROS) level of these cells was determined with 2

7-dichlorofluoresce in diacetate (DCFH-DA) as fluorescence probe

intracellular NO level by Greiss method

intracellular iNOS protein and cytoplasmic/nuclear Nrf2 protein expression by Western blotting

and mRNA expression of heme oxygenase-1 (HO-1) by RT-PCR.       Results      Compared with the control group

LPS significantly induced the levels of ROS

NO and iNOS protein in RAW264.7 cells

and AGM significantly reversed such effect (P0.05). Nrf2 pathway and its target HO-1 were significantly up-regulated compared to LPS-stimulated cells

suggesting that AGM activated the Nrf2 signaling pathway.       Conclusion      AGM reduces oxidative damage of the RAW264.7 cells by promoting HO-1 antioxidase expression through activation of the Nrf2 pathway.