Sulforaphane suppressed LPS-induced inflammation in mouse peritoneal macrophages through Nrf2 dependent pathway |
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| Authors: | Lin Wen Wu Rachel T Wu Tienyuan Khor Tin-Oo Wang Hu Kong Ah-Ng |
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| Institution: | a Graduate Program in Pharmaceutical Science, Rutgers, The State University of New Jersey, Piscataway, NJ, USA
b Department of Pharmaceutics, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, NJ, USA |
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| Abstract: | Sulforaphane (SFN) is a natural isothiocyanate that is present in cruciferous vegetables such as broccoli and cabbage. Previous studies have shown that SFN is effective in preventing carcinogenesis induced by carcinogens in rodents, which is related in part to its potent anti-inflammation properties. In the present study, we compared the anti-inflammatory effect of SFN on LPS-stimulated inflammation in primary peritoneal macrophages derived from Nrf2 (+/+) and Nrf2 (−/−) mice. Pretreatment of SFN in Nrf2 (+/+) primary peritoneal macrophages potently inhibited LPS-stimulated mRNA expression, protein expression and production of TNF-α, IL-1β, COX-2 and iNOS. HO-1 expression was significantly augmented in LPS-stimulated Nrf2 (+/+) primary peritoneal macrophages by SFN. Interestingly, the anti-inflammatory effect was attenuated in Nrf2 (−/−) primary peritoneal macrophages. We concluded that SFN exerts its anti-inflammatory activity mainly via activation of Nrf2 in mouse peritoneal macrophages. |
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| Keywords: | SFN sulforaphane COX-2 cyclooxygenase-2 IL-1β interleukin-1β iNOS inducible nitric oxide synthase NF-κB nuclear 3 factor-κB Nrf2 nuclear E2-factor related factor 2 PGE2 prostaglandin E2 TNF-α tumor necrosis factor-α |
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