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Regulation of Inflammatory Cytokine Production by Bee Venom in Rat Chondrocytes
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  • Regulation of Inflammatory Cytokine Production by Bee Venom in Rat Chondrocytes
  • Regulation of Inflammatory Cytokine Production by Bee Venom in Rat Chondrocytes
저자명
Kim. Eun-Jung,Kim. Gye-Yeop
간행물명
동의생리병리학회지
권/호정보
2011년|25권 1호|pp.132-137 (6 pages)
발행정보
대한동의생리학회
파일정보
정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
서지반출

기타언어초록

Bee venom acupuncture (BVA), as a kind of herbal acupuncture, involved injecting diluted bee venom into acupoints and is used for pain, osteoarthritis and rheumatoid arthritis patients. BVA is growing in popularity, especially in Korea, and is used primarily for pain relief in many kinds of diseases. However, the effect of bee venom anti-inflammatory related action in lipopolysaccharide (LPS) induced chondrocyte stress have not been reported yet. The aim of this study was to investigate the effect of bee venom of cell viability and inflammatory cytokine in rat articular chondrocyte cultures stimulated with lipopolysaccharide. Inflammation was induced in rat chondrocytes by treatment with $10{mu}g/m{ell}$ LPS. The change of cell viability were decreased in chondrocytes after treatment with lipopolysaccharide. The cell viability revealed that BV exerted no significant cytotoxicity in the rat chondrocyte. Bee venom inhibited decreased cell viability in the presence of lipopolysaccharide ($10{mu}g/m{ell}$) in a dose dependent manner(0.1, 0.5, 1.0 and $5.0{mu}g/m{ell}$) at bee venom(p<0.05). Tumor necrosis factor (TNF)-${alpha}$ production in the presence of lipopolysaccharide($1{mu}g/m{ell}$) was also inhibited in a dose dependent manner (p<0.05 from bee venom $0.1{mu}g/m{ell}$). Interleukin (IL)-6 production in the presence of lipopolysaccharide ($10{mu}g/m{ell}$) was inhibited as well (p<0.05 at bee venom 0.1, 0.5, 1.0 and $5.0{mu}g/m{ell}$, respectively). Our results demonstrate that bee venom was a anti-inflammatory agent of chondrocytes. Bee venom may exert its anti inflammatory effects through inhibition of TNF-${alpha}$ and IL-6 synthesis, and may then pain relief and reduce the articular destruction.