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Coenzyme Q0

CAS No. : 605-94-7

MCE 国际站：Coenzyme Q0

产品活性：Coenzyme Q0 (CoQ0) 是一种口服有效的醌类化合物，可以从 Antrodia cinnamomea 中得到。Coenzyme Q0 诱导细胞凋亡 (apoptosis) 和自噬 (autophagy)，抑制 HER-2/AKT/mTOR 信号通路来增强细胞凋亡和自噬机制。Coenzyme Q0 调节 NFκB/AP-1 的激活，并增强 Nrf2 的稳定，减轻炎症和氧化还原失衡。Coenzyme Q0 通过下调 MMP-9/NF-κB 和上调 HO-1 信号通路具有抗血管生成活性。

研究领域：Apoptosis  |  Autophagy  |  JAK/STAT Signaling  |  Protein Tyrosine Kinase/RTK  |  PI3K/Akt/mTOR  |  Immunology/Inflammation  |  NF-κB  |  Metabolic Enzyme/Protease  |  Cell Cycle/DNA Damage  |  Epigenetics

作用靶点：Apoptosis  |  Autophagy  |  EGFR  |  Akt  |  mTOR  |  Caspase  |  Bcl-2 Family  |  Reactive Oxygen Species  |  PARP  |  COX  |  NO Synthase  |  TNF Receptor  |  Interleukin Related  |  MMP  |  NF-κB

In Vitro: Coenzyme Q0 (0-40 µM; 24 h) and inhibits viability and growth of human ovarian carcinoma cells.
Coenzyme Q0 (CoQ0) (0-30 µM; 24 h; SKOV-3 cells) has anti-proliferative activity through induction of G2/M cell-cycle arrest and reduction of cell-cycle regulatory proteins.
Coenzyme Q0 (CoQ0) (0-30 µM; 0-30 min; SKOV-3 cells) increases intracellular ROS levels to promote SKOV-3 cell death.
Coenzyme Q0 (CoQ0) (0-30 µM; 24 h; SKOV-3 cells) induces autophagy by increase accumulation of LC3-II, GFP-LC3 puncta, AVOs formation and Beclin-1/Bcl-2 dysregulation.
Coenzyme Q0 (CoQ0) (0-30 µM; 24 h; SKOV-3 cells) induces apoptosis by mitochondrial (caspase-3, PARP and Bax/Bcl-2 dysregulation) and ER stress (caspase-12 and Hsp70) signals.
Coenzyme Q0 (CoQ0) (30 µM; 24 h; SKOV-3 cells) suppresses of HER-2/AKT/mTOR signaling to potentiate the apoptosis and autophagy mechanisms.
Coenzyme Q0 (CoQ0) (0-10 µM; 0.5-18 h; RAW264.7 cells) regulates NFκB/AP-1 activation and enhances Nrf2 stabilization.
Coenzyme Q0 (CoQ0) (5 µM; 0-12 h; EA.hy 926 cells) has anti-angiogenic activity in EA.hy 926 cells.

In Vivo: Coenzyme Q0 (CoQ0) (1.5 and 2.5 mg/kg; i.p.; once every four days, for 52 d) suppresses tumor growth in SKOV-3 xenografted nude mice.
Coenzyme Q0(CoQ0) (5 mg/kg; p.o.; for 4 h) has anti-inflammatory activities through Nrf2 activation and NFκB inhibition in liver and spleen of LPS-treated mice.

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