NF-κB와 MAPK 억제를 통한 스테비아 잎의 항염증효과
Anti-inflammatory Effect of Stevia Rebaudiana as a Results of NF-κB and MAPK Inhibition
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Objectives : Stevia rebaudiana is a well-known herbal sweetener in the Korea, Japan and China, and its medical uses were originated from countries in South America. Although it has been shown the various medical effects of S. rebaudiana including contraception and treatment of human diseases such as hyperglycemia, it has almost not been studied about the efficacy of S. rebaudiana methanolic extract (SRE) on the acute inflammation and its action mechanism. Methods : To investigate the anti-inflammatory effects of SRE, we treated SRE and examined the level of inflammatory mediators in LPS-stimulated Raw264.7 cells. Results : Treatment of macrophage with LPS markedly induced the production of NO, PGE2 and pro-inflammatory cytokines. Pretreatment of SRE blocked the induction of inflammatory mediators and the expression of iNOS protein. More importantly, LPS-induced phosphorylation of IκB-α was suppressed by the treatment of SRE,suggesting SRE inhibition of NF-κB activation. Furthermore, SRE blocked LPS-induced phosphorylation of MAPKs. Conclusions : SRE inhibited the induction of NO, PGE2 and pro-inflammatory cytokines in Raw264.7 cells. SRE's effect may be mediated with its inhibition of NF-κB activation and MAPK phosphorylation, which suggests its uses as an anti-inflammatory agents.
Abstract
Objectives : Stevia rebaudiana is a well-known herbal sweetener in the Korea, Japan and China, and its medical uses were originated from countries in South America. Although it has been shown the various medical effects of S. rebaudiana including contraception and treatment of human diseases such as hyperglycemia, it has almost not been studied about the efficacy of S. rebaudiana methanolic extract (SRE) on the acute inflammation and its action mechanism. Methods : To investigate the anti-inflammatory effects of SRE, we treated SRE and examined the level of inflammatory mediators in LPS-stimulated Raw264.7 cells. Results : Treatment of macrophage with LPS markedly induced the production of NO, PGE2 and pro-inflammatory cytokines. Pretreatment of SRE blocked the induction of inflammatory mediators and the expression of iNOS protein. More importantly, LPS-induced phosphorylation of IκB-α was suppressed by the treatment of SRE,suggesting SRE inhibition of NF-κB activation. Furthermore, SRE blocked LPS-induced phosphorylation of MAPKs. Conclusions : SRE inhibited the induction of NO, PGE2 and pro-inflammatory cytokines in Raw264.7 cells. SRE's effect may be mediated with its inhibition of NF-κB activation and MAPK phosphorylation, which suggests its uses as an anti-inflammatory agents.
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