(-)-Butin

(-)-Butin (Butin) 是 Butin 的 S 对映体。其中 Butin 是一种分离自黄檀的心材中的生物活性黄酮类化合物,具有显著的抗血小板、抗氧化、抗炎作用。

CAS号

492-14-8

分子式

C15H12O5

主要靶点

Akt|PI3K|Nrf2

仅限科研使用

Cat No : CM12556

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Synonyms

Butin|漆黄素 ( 紫铆素)



产品信息

(-)-Butin has antioxidant activity, can protect cells against H2O2-induced apoptosis, oxidative DNA damage and oxidative mitochondrial dysfunction; it attenuates oxidative stress by activating Nrf2-mediated Mn SOD induction via the PI3K/Akt signaling pathway.

CAS号 492-14-8
分子式 C15H12O5
主要靶点 Akt|PI3K|Nrf2
主要通路 细胞骨架|免疫与炎症|PI3K/Akt/mTOR信号通路
分子量 272.25
纯度 98.07%, 此纯度可做参考,具体纯度与批次有关系,可咨询客服
储存条件 Powder: -20°C for 3 years | In solvent: -80°C for 1 year
别名 Butin|漆黄素 ( 紫铆素)

体外活性

The antioxidant function of manganese superoxide dismutase (Mn SOD) is important in preventing oxidative stress. While exposure to H2O2 reduced the expression of Mn SOD in Chinese hamster lung fibroblast (V79-4), the addition of Butin restored Mn SOD expression at both the mRNA and protein levels, resulting in increased Mn SOD activity. The transcription factor NF-E2-related factor 2 (Nrf2) regulates Mn SOD gene expression by binding to the antioxidant responsive element (ARE). Butin enhanced the nuclear translocation and ARE-binding activity of Nrf2, which was decreased by H2O2. The siRNA-mediated knockdown of Nrf2 attenuated Butin-induced Mn SOD expression and activity. Further, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB, Akt) contributed to the ARE-driven Mn SOD expression. Butin activated PI3K/Akt and exposure to either LY294002 (a PI3K inhibitor), Akt inhibitor IV (an Akt-specific inhibitor), or Akt siRNA suppressed the Butin-induced activation of Nrf2, resulting in decreased Mn SOD expression and activity. Finally, the cytoprotective effect of Butin against H2O2-induced cell damage was suppressed by the siRNA-mediated knockdown of Mn SOD[1]

溶解度

DMSO:50 mg/mL (183.65 mM)

参考文献

1.The cytoprotective effect of butin against oxidative stress is mediated by the up-regulation of manganese superoxide dismutase expression through a PI3K/Akt/Nrf2-dependent pathway.J Cell Biochem. 2012 Jun;113(6):1987-97.

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