Eurycomanone and eurycomanol from Eurycoma longifolia Jack as regulators of signaling pathways involved in proliferation, cell death and inflammation.

Eurycomanone and eurycomanol from Eurycoma longifolia Jack as regulators of signaling pathways involved in proliferation, cell death and inflammation.
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DOI:
10.3390/molecules190914649
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发表时间:
2014-09-16
期刊:
Molecules (Basel, Switzerland)
影响因子:
--
通讯作者:
Diederich M
Diederich M
中科院分区:
其他
文献类型:
--
作者:
Hajjouli S;Chateauvieux S;Teiten MH;Orlikova B;Schumacher M;Dicato M;Choo CY;Diederich M

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Eurycomanone和Eurycomanol是从东革阿里(Eurycoma longifolia Jack)根中分离得到的两个苦木素类化合物。本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核细胞相比的生物活性。eurycomanone和eurycomanol都抑制Jurkat和K562细胞的活力和增殖,而不影响健康细胞。有趣的是,eurycomanone通过抑制IκBα磷酸化和上游丝裂原活化蛋白激酶(MAPK)信号传导抑制NF-κB信号传导,而不是eurycomanol。总之,两种苦木素类化合物对白血病细胞具有不同的毒性,并且eurycomanone中α,β-不饱和酮的存在可能是NF-κB抑制的先决条件。
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-κB signaling through inhibition of IκBα 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 α,β-unsaturated ketone in eurycomanone could be prerequisite for the NF-κB inhibition.
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