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NF-kB and AP-1-regulatory Mechanism of Buthus Martensi Karsch Herbal Acupuncture Solution on Inflammatory Cytokine-induced Human Chondrocytes Dysfunction
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  • NF-kB and AP-1-regulatory Mechanism of Buthus Martensi Karsch Herbal Acupuncture Solution on Inflammatory Cytokine-induced Human Chondrocytes Dysfunction
  • NF-kB and AP-1-regulatory Mechanism of Buthus Martensi Karsch Herbal Acupuncture Solution on Inflammatory Cytokine-induced Human Chondrocytes Dysfunction
저자명
Cho. Jae-Yong,Kim. Kyung-Ho,Cho. Hyun-Seok,Lim. Dae-Jung,Hwang. Ji-Hye,Kim. Kap-Sung
간행물명
大韓鍼灸學會誌= The journal of Korean Acupuncture & Moxibustion Society
권/호정보
2006년|23권 2호|pp.61-72 (12 pages)
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대한침구학회
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정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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Objectives : Human chondrocytes co-treated with Buthus martensi Karsch herbal acupuncture solution(BMK-HAS) extract produced significantly less NO compared with chondrocytes stimulated with $IL-1{eta}$ alone Methods : Activation and translocation of and NF-kB DNA binding activity were determined by Western blotting and specific enzyme-linked immunosorbent assay. Results : The inhibition of NO production correlated with the suppression of induction and expression of nuclear factor-kB (NF-kB) and activation protein-1 (AP-1)-dependent gene. BMK-HAS inhibited the activation and translocation of NF-kB to the nucleus, indicating that BMK-HAS inhibits the $IL-1{eta}-induced$ production of NO in human chondrocytes by interfering with the activation of NF-kB through a novel mechanism. In addition, BMK-HAS reduced prostaglandin E2 (PGE2)production in mouse peritoneal macrophages stimulated with lipopolysaccharide, whereas no influence on the activity of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2) or cyclooxygenase-1 (COX-1) was observed. My data, therefore, suggest that BMK-HAS may be a therapeutically effective inhibitor of $IL-1{eta}-induced$ inflammatory effects that are dependent on NF-kB activation in human OA chondrocytes. Conclusion : The results indicate that BMK-HAS exerts anti-inflammatory effects related to the inhibition of neutrophil functions and of NO and PGE2 production, which could be due to a decreased expression of iNOS and COX-2 through the transcription factors NF-kB and AP-1.