2. PI3K/Akt/mTOR Stem Cell/Wnt MAPK/ERK Pathway Metabolic Enzyme/Protease NF-κB Immunology/Inflammation
  3. Akt ERK p38 MAPK MMP NADPH Oxidase Reactive Oxygen Species (ROS) Keap1-Nrf2
  4. Adonixanthin

Adonixanthin  (Synonyms: (3S,3′R)-Adonixanthin)

目录号: HY-W750654
产品使用指南 技术支持

Adonixanthin ((3S,3'R)-Adonixanthin), 是一种类胡萝卜素并且是一种具有口服活性的抗氧化和抗癌剂。Adonixanthin 具有抑制三种胶质母细胞瘤细胞增殖和迁移的能力。Adonixanthin 对多种类型的损伤都具有细胞保护作用，并能抑制活性氧 (ROS) 产生的增加。Adonixanthin不仅通过抗氧化反应，还通过激活 Nrf2 来保护细胞免受光诱导的损伤。Adonixanthin 可抑制胶质母细胞瘤的进展，且在自体血脑出血 (ICH) 模型中能改善血脑屏障的高通透性。Adonixanthin 可用于胶质母细胞瘤 (GBM) 和脑出血 (ICH) 的研究。

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Adonixanthin

Adonixanthin Chemical Structure

CAS No. : 4418-73-9

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Adonixanthin 相关抗体

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

Adonixanthin ( (3S,3'R)-Adonixanthin), a carotenoid, is an orally active anti-oxidative and anti-carcinogenic agent. Adonixanthin shows an ability to suppress cell proliferation and migration in three types of glioblastoma cells Adonixanthin exerts cytoprotective effects against various types of damage and inhibits the increased production of ROS. Adonixanthin protects against light-induced cell damage through not only an anti-oxidative response but also through Nrf2 activation. Adonixanthin suppresses glioblastoma progression and adonixanthin improves blood-brain barrier hyper-permeability in an autologous blood ICH model. Adonixanthin can be used for the study of glioblastoma (GBM) and intracerebral hemorrhage (ICH)[1].

体外研究
(In Vitro)

Adonixanthin (0.1-10 μM, 96 h) 抑制小鼠胶质母细胞瘤细胞系 GL261 和人胶质母细胞瘤细胞系 U251MG 的增殖[1]。
Adonixanthin (10 μM, 72 h) 降低 GL261 细胞中 BrdU 阳性细胞的比例[1]。
Adonixanthin (10 μM, 48 h) 抑制 GL261 和 U251MG 细胞的迁移[1]。
Adonixanthin (10 μM, 6 h) 降低 GL261 细胞中 p-ERK1/2 和 p-Akt 的磷酸化水平[1]。
Adonixanthin (10 μM, 6-48 h) 增加 GL261 细胞中 p-p38 的磷酸化，降低 cyclin D1 的表达，增加 p27 的表达，降低 MMP-2、Nox4 和纤维连接蛋白的表达，对 MMP-9 无显著影响[1]。
Adonixanthin (0.1-1 µM, 4 h) 显著减少人脑内皮细胞 (HBMVECs) 中血红蛋白诱导的细胞死亡和 ROS 产生，并上调 HO-1 和 VE-钙粘蛋白水平[2]。
Adonixanthin (0.1-1 µM, 28 h) 显著减少 HBMVECs 中胶原酶诱导的细胞死亡，抑制 ERK1/2 磷酸化，并上调 VE-钙粘蛋白水平[2]。
Adonixanthin (0.1-1 µM, 25 h) 呈浓度依赖性减少 SH-SY5Y 细胞中 H2O2 诱导和 LPS 诱导的细胞死亡[2]。
Adonixanthin 在摩尔比/Hyptadienic acid (TPA) 为 329 的半数抑制浓度下，抑制 Raji 细胞中 Epstein-Barr 病毒早期抗原的激活，且无显著细胞毒性[3]。
Adonixanthin (167 μM) 抑制 AMVN 诱导的亚油酸甲酯过氧化[3]。
Adonixanthin (1-100 μM) 在乙醇中的亚甲基蓝敏化光氧化体系中具有单线态氧淬灭活性，半数抑制浓度为 11.1 μM[3]。
Adonixanthin (20 μM, 6 h) 可上调 661 W 细胞中 Nrf2 调控基因的 mRNA 表达，并增加细胞核中的Nrf2[4]。
Adonixanthin (10 μM) 可保护 661 W 细胞免受光诱导的细胞死亡，并减少光暴露诱导的活性氧产生，而 Nrf2 沉默会消除这种作用[4]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Adonixanthin 相关抗体:

Cell Migration Assay [1]

Cell Line: GL261 and U251MG cells
Concentration: 10 μM
Incubation Time: 48 h
Result: Suppressed the migration of GL261 and U251MG cells.

Western Blot Analysis[1]

Cell Line: GL261 cells
Concentration: 10 μM
Incubation Time: 6, 48 h
Result: Decreased the phosphorylation levels of p-ERK1/2 and p-Akt.
Increased p-p38 phosphorylation.
Reduced cyclin D1 expression.
Increased p27 expression.
Decreased the expression of MMP-2, fibronectin and Nox4.

Western Blot Analysis[2]

Cell Line: human brain endothelial cells (HBMVECs)
Concentration: 1 μM
Incubation Time: 28 h
Result: Inhibited ERK1/2 phosphorylation.
Upregulated VE-cadherin levels.

Real Time qPCR[4]

Cell Line: 661 W cells
Concentration: 20 μM
Incubation Time: 6 h
Result: Upregulated the mRNA expression of Nrf2-controlled genes Ho-1, Nqo-1, and Gclm.
体内研究
(In Vivo)

Adonixanthin (10-30 mg/kg, 口服, 每日一次, 持续 10 天) 可显著抑制 C57BL/6J 小鼠原位胶质母细胞瘤的进展[1]。
Adonixanthin (100 mg/kg, 口服, 每日一次, 持续 7 天) 可改善自体血注射脑出血模型小鼠的血脑屏障高通透性[2]。
Adonixanthin (50 μg (85 nmol), 局部涂抹, 每次 TPA 处理前 1 小时给药, 持续 20 周) 可显著降低由 DMBA (HY-W011845) 启动、Hyptadienic acid (TPA) (HY-N4024) 促进的小鼠皮肤癌模型中乳头状瘤的发生率和数量[3]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: GL261 cells (1 × 105 in 2 µL PBS) were intracranially implanted into male C57BL/6J mice (8 weeks old; body weight 22-27 g))[1]
Dosage: 10, 30 mg/kg
Administration: p.o. once daily for 10 days
Result: Suppressed tumour progression and reduced tumour area and volume.
Showed no significant effect on body weight.
Animal Model: Male ddY mice aged 8-9 weeks were administered twenty-five microliters of blood over 5 min, with the needle left in place for 3 min and then slowly removed over 2 min[2]
Dosage: 100 mg/kg
Administration: p.o. once daily for 7 days until 12 h before ICH induction
Result: Improves blood-brain barrier hyperpermeability.
Reduced Evans blue leakage.
Ameliorated neurological deficits.
Increased Garcia scores.
Reduced the number of limb errors in the grid walk test.
Animal Model: ICR mice (6-week old) were treated with DMBA (100 μg, 390 nmol in 0.1 mL acetone) as the initiator applied topically one week before the first promotion[3]
Dosage: 50 μg (85 nmol) dissolved in 0.1 mL acetone
Administration: Applied topically to the shaved backs of mice 1 h before each Hyptadienic acid (TPA) (HY-N4024) treatment twice a week for 20 weeks
Result: Delayed the formation of papillomas.
Reduced the number of papillomas per mouse in DMBA-initiated and TPA-promoted mouse skin carcinogenesis.
分子量

582.85

Formula

C40H54O3
CAS 号
结构分类
初始来源

marine bacterium strain SD-212
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

Adonixanthin 相关分类

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Keywords:

Adonixanthin4418-73-9(3S,3′R)-AdonixanthinAktERKp38 MAPKMMPNADPH OxidaseReactive Oxygen Species (ROS)Keap1-Nrf2PKBProtein kinase BExtracellular signal regulated kinasesMatrix metalloproteinasesNOXglioblastomaintracerebral hemorrhageAKTp38,MMPROSInhibitorinhibitorinhibit

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