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KMID : 0923620110110060420
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Immune Network
2011 Volume.11 No. 6 p.420 ~ p.423
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CKD-712, (S)-1-(?-naphthylmethyl)-6,7-dihydroxy-1,2,3,4- tetrahydroisoquinoline, Inhibits the NF-?B Activation and Augments Akt Activation during TLR4 Signaling
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Lee Jeong-Gi
Yang Eun-Jeong
Shin Jeon-Soo
Kim Dal-Hyun
Lee Sung-Sook
Choi In-Hong
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Abstract
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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-?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-?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-?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.
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KEYWORD
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CKD-712, TLR4, Akt, immunomodulator
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