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2009:
Motoyama Keiichi; Hashimoto Yosuke; Hirayama Fumitoshi; Uekama Kaneto; Arima Hidetoshi
Inhibitory effects of 2,6-di-O-methyl-alpha-cyclodextrin on poly I:C signaling in macrophages.
European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences 2009;
36(
2-3):.
In the present study, we examined the effects of alpha-cyclodextrin (alpha-CyD), 2-hydroxypropyl-alpha-cyclodextrin (HP-alpha-CyD) and 2,6-di-O-methyl-alpha-cyclodextrin (DM-alpha-CyD) on the nitric oxide (NO) and interferon-beta (IFN-beta) production in murine and human macrophages stimulated with Poly I:C and CpG-DNA, toll-like receptor 3 (TLR3) and TLR9 ligands, respectively. DM-alpha-CyD significantly inhibited NO production in RAW264.7 cells and U937 cells differentiated by phorbol myristate acetate (PMA), murine and human macrophage-like cell lines, respectively, stimulated with Poly I:C without cytotoxicity, but neither alpha-CyD nor HP-alpha-CyD did. Meanwhile, the three alpha-CyDs did not inhibit NO production in RAW264.7 cells stimulated with CpG-DNA. DM-alpha-CyD inhibited inducible NO synthase (iNOS) and IFN-beta expression upon stimulation with Poly I:C. Furthermore, DM-alpha-CyD markedly decreased the cellular uptake of Poly I:C in RAW264.7 cells. Therefore, DM-alpha-CyD may be useful as a potent inhibitor for excess activation of macrophages stimulated with Poly I:C.
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