Curcumin decreased level of proinflammatory cytokines in monocyte cultures exposed to preeclamptic plasma by affecting the transcription factors NF-κB and PPAR-γ

The purpose of this study is to determine the role of curcumin in the alteration of levels of interleukin (IL)-1α, IL-6, and tumor necrosis factor α (TNF-α) as proinflammatory cytokines in monocyte culture exposed to preeclamptic plasma, as well as the effect on the transcription factors: nuclear factor kappa beta (NF-κB) and peroxisome proliferator-activated receptor γ (PPAR-γ). Plasma was taken from preeclamptic women (n = 12) and normotensive pregnant women (n = 12). Monocyte cultures were taken from nonpregnant healthy woman. Monocyte cultures were incubated with plasma for 48 hours. Curcumin in various doses were given in monocytic cultures prior to and after preeclamptic plasma exposure. The levels of IL-1α, IL-6, and TNF-α as well as NF-κB and PPAR-γ in each culture were determined by enzyme-linked immunosorbent assay procedures. The final data were analyzed by analysis of variance (ANOVA) and path analysis. This study shows a significant increase (p < 0.05) in the levels of proinflammatory cytokines (IL-1α, IL-6, and TNFα) in monocyte cultures exposed to preeclamptic plasma compared with normotensive pregnancy plasma. Curcumin treatment in various doses can decrease significantly (p < 0.05) proinflammatory cytokine levels in monocyte cultures that have been already stimulated by preeclamptic plasma. After curcumin treatment, there was a decreased level of nuclear NF-κB p50 and a significantly increased level of PPAR-γ. Curcumin has a direct effect on decreasing the levels of nuclear NF-κB p50 and also curcumin indirectly influenced the level of nuclear NF-κB p50 by the increased level of PPAR-γ. Curcumin could decrease levels of proinflammatory cytokines (IL-1α, IL-6, and TNFα) in monocyte cultures exposed to preeclamptic plasma by affecting the transcription factors, NF-κB and PPAR-γ. Curcumin has potential in the prevention and future treatment of preeclampsia, through inflammation pathways assumed as being responsible for the development of preeclampsia.