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  • tert-Butylhydroquinone
  • 叔丁基对苯二酚;TBHQ
  • 货号: abs814799
    CAS号: 1948-33-0
    分子式: C10H14O2
    分子量: 166.22
    产品说明书
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    货号-规格 货期 价格 数量
    abs814799-1g 1-2周 ¥420.00
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    abs814799-5g 现货 ¥840.00
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    大包装询价
    产品描述
    描述

    Tert-butylhydroquinone (TBHQ) is an antioxidant compound which is used to prevent lipid peroxidation and shows multiple cytoprotective actions. It is an activator of Nrf2. 

    纯度
    >98%
    储存/保存方法
    store at -20℃ for one year(Powder); in DMSO or others solvent store at 2-4℃ for two weeks, at -80℃ for six months.
    形态
    Solid
    基本信息
    别名
    叔丁基对苯二酚;TBHQ
    外观
    白色至类白色粉末
    可溶性/溶解性
    DMSO :33 mg/mL (198.53 mM)
    生物活性
    靶点
    Nrf2
    In vitro(体外研究)
    Tert-butylhydroquinone (tBHQ) is a metabolite of the chemical compound butylated hydroxyanisole and induces Nrf2 activation and conveys protection against hydrogen peroxide, 6-hydroxydopamine, the pesticidal deltamethrin, and other toxicants. tBHQ preferentially alters the redox status in the mitochondrial compartment in HeLa cells. HeLa cells treated with tBHQ show a preferential oxidation of mitochondrial thioredoxin-2 (Trx2), while cellular glutathione and cytosolic thioredoxin-1 are not affected. In cultured H9c2 cells and primary cardiac myocytes, TBHQ stimulates Akt phosphorylation and suppresses oxidant-induced apoptosis.
    In vivo(体内研究)
    TBHQ treatment elicits significant cytoprotective actions in different organs under pathological conditions. Systemic or local intra-cerebroventricular treatment with TBHQ in an ischemic stroke model in rats significantly reduces the infarct size and neurological deficits. Administration of TBHQ in rats suppresses renal damage and oxidative stress after ischemia and reperfusion injury. In mice with type 1 diabetes, chronic treatment with TBHQ significantly reduces the degree of glomerular fibrosis and ameliorates proteinuria. TBHQ treatment prevents left ventricular dilatation and cardiac dysfunction induced by transverse aortic constriction (TAC), and decreases the prevalence of myocardial apoptosis. The beneficial effects of TBHQ are associated with an increase in Akt activation, but not related to activations of Nrf2 or AMP-activated protein kinase. TBHQ-induced Akt activation is accompanied by increased phosphorylation of Bad, glycogen synthase kinase-3β (GSK-3β) and mammalian target of rapamycin (mTOR).
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