三七花의 대식세포로부터 LPS에 의해 유도되는 nitric oxide와 전염증성 사이토카인의 생성 억제효과

Objectives: Inflammatory mediators, such as nitric oxide (NO), prostaglandin E2 (PGE2) and pro-inflammatory cytokines, TNF-α and IL-1β play a critical role in inflammatory immune response. Therefore, intervention of inflammatory mediator production promises therapeutic benefit for treatment of many chronic inflammatory diseases, such as allergic asthma, rheumatoid arthritis, multiple sclerosis, septic shock and neurodegenerative diseases. In this study, the pharmacological effects of the flower MeOH extract Panax notoginseng (Notoginseng Flos; NF) on inflammation were investigated to address potential therapeutic or toxic effects. Methods: RAW264.7 cells were treated with different concentrations of NF methanol (NF-M) extract in the presence or absence of LPS (1 ㎍/㎖). Results: NF-M extract significantly inhibited LPS-induced production of NO, PGE2 and pro-inflammatory cytokines, TNF-α and IL-1β in a dose-dependent manner. In addition, NF-M extract suppressed mRNA expressions and protein levels of iNOS, COX-2 and pro-inflammatory cytokines in LPS-stimulated RAW264.7 cells. Conclusion: These results indicated that NF-M extract inhibits LPS-induced production of inflammatory mediators in macrophages and demonstrated that NF-M extract possesses anti-inflammatory properties in vitro. Objectives: Inflammatory mediators, such as nitric oxide (NO), prostaglandin E2 (PGE2) and pro-inflammatory cytokines, TNF-α and IL-1β play a critical role in inflammatory immune response. Therefore, intervention of inflammatory mediator production promises therapeutic benefit for treatment of many chronic inflammatory diseases, such as allergic asthma, rheumatoid arthritis, multiple sclerosis, septic shock and neurodegenerative diseases. In this study, the pharmacological effects of the flower MeOH extract Panax notoginseng (Notoginseng Flos; NF) on inflammation were investigated to address potential therapeutic or toxic effects. Methods: RAW264.7 cells were treated with different concentrations of NF methanol (NF-M) extract in the presence or absence of LPS (1 ㎍/㎖). Results: NF-M extract significantly inhibited LPS-induced production of NO, PGE2 and pro-inflammatory cytokines, TNF-α and IL-1β in a dose-dependent manner. In addition, NF-M extract suppressed mRNA expressions and protein levels of iNOS, COX-2 and pro-inflammatory cytokines in LPS-stimulated RAW264.7 cells. Conclusion: These results indicated that NF-M extract inhibits LPS-induced production of inflammatory mediators