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Schisandrol B五味子醇乙,58546-54-6

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  • ¥273 - 3600
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  • HY-N0692
  • 2025年12月05日
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    • 详细信息
    • 文献和实验
    • 技术资料
    • 保存条件

      Powder: -20°C, 3 years; 4°C, 2 years.In solvent: -80°C, 6 months; -20°C, 1 month.

    • 英文名

      Gomisin-A; TJN-101; Wuweizi alcohol-B

    • 库存

      货期:1-2天

    • 供应商

      MedChemExpress LLC

    • 规格

      10 mM * 1 mL/1 mg/5 mg/10 mg/25 mg/50 mg/100 mg

    规格:10 mM * 1 mL产品价格:¥550.0
    规格:1 mg产品价格:¥273.0
    规格:5 mg产品价格:¥600.0
    规格:10 mg产品价格:¥950.0
    规格:25 mg产品价格:¥1700.0
    规格:50 mg产品价格:¥2550.0
    规格:100 mg产品价格:¥3600.0

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    Schisandrol B

    CAS No. : 58546-54-6

    MCE 国际站:Schisandrol B

    产品活性:Schisandrol B (Gomisin-A) 是 Schisandra chinensis 的主要活性成分,具有保肝作用。Schisandrol B 抑制活性氧 (ROS) 的产生。Schisandrol B 抑制 P-糖蛋白和 CYP3A 的活性,还具有抗炎,抗糖尿病和抗氧化的作用。

    研究领域:Metabolic Enzyme/Protease  |  Immunology/Inflammation  |  NF-κB  |  Autophagy

    作用靶点:Reactive Oxygen Species  |  Cytochrome P450  |  Autophagy

    In Vitro: Schisandrol B (Gomisin-A; 1-10 μM; 2 days) treatment decreases the aging related inflammatory molecules, such as, COX-2, IL1β, and TNF-α. Schisandrol B attenuates the activity of senescence-associated β-galactosidase.
    Schisandrol B (Gomisin-A; 1-10 μM; 2 days) inhibits reactive oxygen species production even in the stress-induced premature senescence (SIPS)-human diploid fibroblast (HDF) cells.
    Schisandrol B (Gomisin-A; 1-10 μM) inhibits the MAPK pathway and the translocation of NF-κB to the nucleus.
    Schisandrol B (Gomisin-A; 1-10 μM) promotes the autophagy and mitochondrial biogenesis factors through the translocation of Nrf-2, and inhibits aging progression in the SIPS-HDF cells.
    Schisandrol B (0-80 μM) dramatically alters APAP metabolic activation by inhibiting the activities of CYP2E1 and CYP3A11.

    In Vivo: Schisandrol B (12.5 -200 mg/kg; oral administration; seven times with an interval of 12 hours) pretreatment significantly attenuates the increases in alanine aminotransferase and aspartate aminotransferase activity, and prevents elevated hepatic malondialdehyde formation and the depletion of GSH in a dose-dependent manner. Schisandrol B abrogates APAP-induced activation of p53 and p21, and increases expression of liver regeneration and antiapoptotic-related proteins such as cyclin D1 (CCND1), PCNA, and BCL-2.

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