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Eurycomanone and Eurycomanol from Eurycoma longifolia Jack as Regulators of Signaling Pathways Involved in Proliferation, Cell Death and Inflammation

机译:Eurycoma longifolia Jack的Eurycomanone和Eurycomanol用作增殖,细胞死亡和炎症信号通路的调节剂

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摘要

Eurycomanone and eurycomanol are two quassinoids from the roots of Eurycoma longifolia Jack. The aim of this study was to assess the bioactivity of these compounds in Jurkat and K562 human leukemia cell models compared to peripheral blood mononuclear cells from healthy donors. Both eurycomanone and eurycomanol inhibited Jurkat and K562 cell viability and proliferation without affecting healthy cells. Interestingly, eurycomanone inhibited NF-kappa B signaling through inhibition of I kappa B alpha phosphorylation and upstream mitogen activated protein kinase (MAPK) signaling, but not eurycomanol. In conclusion, both quassinoids present differential toxicity towards leukemia cells, and the presence of the alpha,beta-unsaturated ketone in eurycomanone could be prerequisite for the NF-kappa B inhibition.
机译:Eurycomanone和eurycomanol是从Eurycoma longifolia Jack的根中提取的两个类quassinoids。这项研究的目的是评估这些化合物在Jurkat和K562人白血病细胞模型中与来自健康供体的外周血单个核细胞相比的生物活性。 eurycomanone和eurycomanol均抑制Jurkat和K562细胞的活力和增殖,而不会影响健康细胞。有趣的是,eurycomanone通过抑制I kappa Bα磷酸化和上游有丝分裂原激活的蛋白激酶(MAPK)信号传导来抑制NF-κB信号传导,但对eurycomanol却没有。总之,两种类胡萝卜素对白血病细胞均表现出不同的毒性作用,而在神经叶酮中抑制α,β-不饱和酮可能是抑制NF-κB的先决条件。

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