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Journal of Cancer Prevention

Original Article

Cancer prevention research 2010; 15(2): 138-142

Published online June 30, 2010

© Korean Society of Cancer Prevention

Tamoxifen Suppresses Inducible Nitric Oxide Synthase Expression in Mouse Macrophages

Earl Han1, Eunyoung Ha2, Sung-Hoon Kim3, Joo-Ho Chung1, Hyung Hwan Baik4 and Ju Yeon Ban5

Abstract

Excessive nitric oxide (NO) production by inducible NO synthase (iNOS) in stimulated inflammatory cells is thought to be a causative factor of cellular injury. In recent studies, it has been shown that tamoxifen, an anti-breast cancer drug, exhibits anti-inflammatory effects. Thus, we investigated the effects of tamoxifen on the production and expression of iNos in lipopolysaccharide (LPS)-activated RAW264.7 macrophages. NO production was assessed by nitrite assay and iNos expression was identified by reverse transcription-polymerase chain reaction (RT-PCR). Activation of nuclear factor-Պb (NfՊb) was determined by electrophoretic mobility shift assay (EMSA). The NO production induced by LPS was markedly reduced by tamoxifen. Tamoxifen also suppressed the LPS-activated expression of iNos mRNA and blocked the LPS-induced activation of NfՊb. The phosphorylation level of extracellular signal-regulated kinase 1/2 (Erk) mitogen-activated protein kinase (MAPK) was not affected by tamoxifen, but the phosphorylation level of p38 MAPK was decreased by tamoxifen. Taken together, the results suggest that tamoxifen inhibits LPS-activated NO production via inhibition of p38 MAPK and NfՊb pathways in RAW264.7 macrophage cells. The results of our study provide evidence that tamoxifen possesses an anti-inflammatory effect. (Cancer Prev Res 15, 138-142, 2010)

Keywords: Tamoxifen, Nitric oxide, Inducible nitric oxide synthase, Inflammation, Macrophage

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