Bisdemethoxycurcumin and Its Cyclized Pyrazole Analogue Differentially Disrupt Lipopolysaccharide Signalling in Human Monocyte-Derived Macrophages.

Pretreatment with dexa significantly prevented the upregulation of M1 (CD80 + /CCR2 + ) cells induced by LPS (0.7 ± 0.3% versus 3.0 ± 1.0%, p < 0.05, n = 6; Figures 2(a) and 2(b) ), whereas a nonsignificant trend of inhibition was observed for GG9 and CLI-095.

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While GG6 reduced LPS-induced I κ B- α degradation and showed a trend towards reduced interleukin-1 β release, GG9 prevented the increase in proinflammatory CD80 + macrophage subset, downregulation of the anti-inflammatory CD206 + /CD163 + subset, increase in p38 phosphorylation, and increase in cell-bound and secreted interleukin-1 β stimulated by LPS, at least in part through signalling pathways not involving Toll-like receptor 4 and nuclear factor- κ B.

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