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KMID : 1140120100150020138
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Cancer Prevention Research
2010 Volume.15 No. 2 p.138 ~ p.142
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Tamoxifen Suppresses Inducible Nitric Oxide Synthase Expression in Mouse Macrophages
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Han Earl
Ha Eun-Young
Kim Sung-Hoon
Chung Joo-Ho
Baik Hyung-Hwan
Ban Ju-Yeon
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Abstract
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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-κb (Nfκb) 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 Nfκb. 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 Nfκb pathways in RAW264.7 macrophage cells. The results of our study provide evidence that tamoxifen possesses an anti-inflammatory effect.
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KEYWORD
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Tamoxifen, Nitric oxide, Inducible nitric oxide synthase, Inflammation, Macrophage
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