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Agastache rugosa Leaf Extract Inhibits the iNOS Expression in ROS 17/2.8 Cells Activated with TNF-$alpha$ and IL-$eta$
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  • Agastache rugosa Leaf Extract Inhibits the iNOS Expression in ROS 17/2.8 Cells Activated with TNF-$alpha$ and IL-$eta$
저자명
Oh. Hwa Min,Kang. Young Jin,Kim. Sun Hee,Lee. Young Soo,Park. Min Kyu,Heo. Ja Myung,Sun. Jin Ji,Kim. Hyo Jung,Kang. Eun Sil,Kim.
간행물명
Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea
권/호정보
2005년|28권 3호|pp.305-310 (6 pages)
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대한약학회
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

It has been suggested that nitric oxide (NO) derived from inducible nitric oxide synthase (iNOS) may act as a mediator of cytokine-induced effects on bone turn-over. NO is also recognized as an important factor in bone remodeling, i.e., participating in osteoblast apoptosis in an arthritic joint. The components of Agastache rugosa are known to have many pharmacological activities. In the present study, we investigated the effects of Agastache rugosa leaf extract (ELAR) on NO production and the iNOS expression in ROS 17/2.8 cells activated by a mixture of inflammatory cytokines including TNF-$alpha$ and IL-1$eta$. A preincubation with ELAR significantly and concentration-dependently reduced the expression of iNOS protein in ROS 17/2.8 cells activated with the cytokine mixture. Consequently, the NO production was also significantly reduced by ELAR with an IC$_{50}$ of 0.75 mg/mL. The inhibitory mechanism of iNOS induction by ELAR prevented the activation and translocation of NF-$kappa$B (p65) to the nucleus from the cytosol fraction. Furthermore, ELAR concentration-dependently reduced the cellular toxicity induced by sodium nitroprusside, an NO-donor. These results suggest that ELAR may be beneficial in NO-mediated inflammatory conditions such as osteoporosis.