产品
编 号：F423095
分子式：C21H22O5
分子量：354.4
分子式：C21H22O5
分子量：354.4
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
5mg
560
In-stock
10mg
880
In-stock
25mg
1760
In-stock
结构图
CAS No: 6754-58-1
产品详情
生物活性：
Xanthohumol is one of the principal flavonoids isolated from hops, the inhibitor of diacylglycerol acetyltransferase (DGAT), COX-1 and COX-2, and shows anti-cancer and anti-angiogenic activities. Xanthohumol also has antiviral activity against bovine viral diarrhea virus (BVDV), rhinovirus, HSV-1, HSV-2 and cytomegalovirus (CMV).
体外研究：
Xanthohumol significantly attenuates ADP-induced blood platelet aggregation, and significantly reduces the expression of fibrinogen receptor (activated form of GPIIbIIIa) on platelets' surface.Xanthohumol (5-50 nM) reduces the frequency of spontaneously occurring Ca2+ sparks and Ca2+ waves in control myocytes and in cells subjected to Ca2+ overload caused by: (1) exposure to low K+ solutions, (2) periods of high frequency electrical stimulation, (3) exposures to isoproterenol or (4) caffeine. Xanthohumol (50-100 nM) reduces the rate of relaxation of electrically- or caffeine-triggered Ca2+ transients, without suppressing ICa, but this effect is small and reversed by isoproterenol at physiological temperatures. Xanthohumol also suppresses the Ca2+ content of the SR, and its rate of recirculation. Treatment of endothelial cells with Xanthohumol leads to increased AMPK phosphorylation and activity. Functional studies using biochemical approaches confirm that AMPK mediates Xanthohumol anti-angiogenic activity. AMPK activation by Xanthohumol is mediated by CAMMKβ, but not LKB1. Analysis of the downstream mechanisms shows that Xanthohumol-induced AMPK activation reduces nitric oxide (NO) levels in endothelial cells by decreasing eNOS phosphorylation. Finally, AKT pathway is inactivated by Xanthohumol as part of its anti-angiogenic activity, but independently from AMPK, suggesting that these two signaling pathways proceed autonomously.Xanthohumol significantly reduces cell viability and induces apoptosis via pro-caspase-3/8 cleavage and poly(ADP ribose) polymerase (PARP) degradation. Pro-caspase-9 cleavage, Bcl2 family expression changes, mitochondrial dysfunction, and intracellular ROS generation also participate in Xanthohumol-induced glioma cell death. Xanthohumol's inhibition of the IGFBP2/AKT/Bcl2 pathway via miR-204-3p targeting plays a critical role in mediating glioma cell death.
Xanthohumol is one of the principal flavonoids isolated from hops, the inhibitor of diacylglycerol acetyltransferase (DGAT), COX-1 and COX-2, and shows anti-cancer and anti-angiogenic activities. Xanthohumol also has antiviral activity against bovine viral diarrhea virus (BVDV), rhinovirus, HSV-1, HSV-2 and cytomegalovirus (CMV).
体外研究：
Xanthohumol significantly attenuates ADP-induced blood platelet aggregation, and significantly reduces the expression of fibrinogen receptor (activated form of GPIIbIIIa) on platelets' surface.Xanthohumol (5-50 nM) reduces the frequency of spontaneously occurring Ca2+ sparks and Ca2+ waves in control myocytes and in cells subjected to Ca2+ overload caused by: (1) exposure to low K+ solutions, (2) periods of high frequency electrical stimulation, (3) exposures to isoproterenol or (4) caffeine. Xanthohumol (50-100 nM) reduces the rate of relaxation of electrically- or caffeine-triggered Ca2+ transients, without suppressing ICa, but this effect is small and reversed by isoproterenol at physiological temperatures. Xanthohumol also suppresses the Ca2+ content of the SR, and its rate of recirculation. Treatment of endothelial cells with Xanthohumol leads to increased AMPK phosphorylation and activity. Functional studies using biochemical approaches confirm that AMPK mediates Xanthohumol anti-angiogenic activity. AMPK activation by Xanthohumol is mediated by CAMMKβ, but not LKB1. Analysis of the downstream mechanisms shows that Xanthohumol-induced AMPK activation reduces nitric oxide (NO) levels in endothelial cells by decreasing eNOS phosphorylation. Finally, AKT pathway is inactivated by Xanthohumol as part of its anti-angiogenic activity, but independently from AMPK, suggesting that these two signaling pathways proceed autonomously.Xanthohumol significantly reduces cell viability and induces apoptosis via pro-caspase-3/8 cleavage and poly(ADP ribose) polymerase (PARP) degradation. Pro-caspase-9 cleavage, Bcl2 family expression changes, mitochondrial dysfunction, and intracellular ROS generation also participate in Xanthohumol-induced glioma cell death. Xanthohumol's inhibition of the IGFBP2/AKT/Bcl2 pathway via miR-204-3p targeting plays a critical role in mediating glioma cell death.
产品资料
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