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서지반출
CKD-712, (S)-1-(${alpha}$-naphthylmethyl)-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, Inhibits the NF-${kappa}B$ Activation and Augments Akt Activation during TLR4 Signaling
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  • CKD-712, (S)-1-(${alpha}$-naphthylmethyl)-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, Inhibits the NF-${kappa}B$ Activation and Augments Akt Activation during TLR4 Signaling
  • CKD-712, (S)-1-(${alpha}$-naphthylmethyl)-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, Inhibits the NF-${kappa}B$ Activation and Augments Akt Activation during TLR4 Signaling
저자명
Lee. Jeong-Gi,Yang. Eun-Jeong,Shin. Jeon-Soo,Kim. Dal-Hyun,Lee. Sung-Sook,Choi. In-Hong
간행물명
Immune network : official journal of the Korean association of immunobiologists
권/호정보
2011년|11권 6호|pp.420-423 (4 pages)
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정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

Since CKD-712 has been developed as an anti-inflammatory agent, we examined the effect of CKD-712 during TLR4 signaling. Using HEK293 cells expressing TLR4, CKD-712 was pre-treated 1 hr before LPS stimulation. Activation of NF-${kappa}B$ was assessed by promoter assay. The activation of ERK, JNK, p38, IRF3 and Akt was measured by western blotting. CKD-712 inhibited the NF-${kappa}B$ signaling triggered by LPS. The activation of ERK, JNK, p38 or IRF3 was not inhibited by CKD-712. On the contrary the activation of these molecules was augmented slightly. The activation of Akt with stimulation of LPS was also enhanced with CKD-712 pre-treatment at lower concentration, but was inhibited at higher concentration. We suggest that during TLR4 signaling CKD-712 inhibits NF-${kappa}B$ activation. However, CKD-712 augmented the activation of Akt as well as Map kinases. Therefore, we suggest that CKD-712 might have a role as an immunomodulator.