产品
编 号：F242180
分子式：C10H14O2
分子量：166.22
分子式：C10H14O2
分子量：166.22
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
352
In-stock
500mg
320
In-stock
1g
400
In-stock
结构图
CAS No: 1948-33-0
产品详情
生物活性：
TBHQ (tert-Butylhydroquinone) is a widely used Nrf2 activator, protects against Doxorubicin (DOX)-induced cardiotoxicity through activation of Nrf2. TBHQ (tert-Butylhydroquinone) is also an ERK activator; rescues Dehydrocorydaline (DHC)-induced cell proliferation inhibitionin melanoma.
体内研究：
TBHQ treatment (50 mg/kg; Intraperitoneal injection; three injections at intervals of 8 h that began 1-h post ICH; CD-1 mice) augments the DNA-Binding activity of Nrf2, attenuates oxidative brain damage and acute neurological deficits afterintracerebral hemorrhage (ICH), attenuates microglial activation with concomitant reduction in the release of proinflammatory cytokine interleukin-1β (IL-1β). TBHQ has the efficacy of post-injury administration in attenuating acute neurological injury after ICH.Animal Model:Male CD-1 mice (8-10 weeks old)
Dosage:50 mg/kg
Administration:Intraperitoneal injection; three injections at intervals of 8 hours that began 1h post ICH.
Result:The treatment augmented the DNA-binding activity of Nrf2, attenuated brain oxidative damage, attenuated the microglial activation and the expression of IL-1β.
体外研究：
TBHQ (t-butylhydroquinone; tBHQ; 0-100 μM; 48 hours; H9c2 cells) alone does not affect H9c2 cells viability. Pre-incubation of the H9c2 cells with various concentrations of tBHQ for 24 hours enhances cell viability which is decreased due to exposure to ethanol in a dose-dependent manner. Treatment with tBHQ markedly enhances the viability of H9c2 cardiomyocytes exposed to ethanol.TBHQ (5 μM; 15 min; H9c2 cells) treatment significantly reduces the amount of apoptotic cells exposed to ethanol.TBHQ (5 μM; H9c2 cells) pre-treatment markedly inhibites the ethanol-induced increase in caspase-3 and Bax expression, and enhances Bcl-2 expression.
TBHQ (tert-Butylhydroquinone) is a widely used Nrf2 activator, protects against Doxorubicin (DOX)-induced cardiotoxicity through activation of Nrf2. TBHQ (tert-Butylhydroquinone) is also an ERK activator; rescues Dehydrocorydaline (DHC)-induced cell proliferation inhibitionin melanoma.
体内研究：
TBHQ treatment (50 mg/kg; Intraperitoneal injection; three injections at intervals of 8 h that began 1-h post ICH; CD-1 mice) augments the DNA-Binding activity of Nrf2, attenuates oxidative brain damage and acute neurological deficits afterintracerebral hemorrhage (ICH), attenuates microglial activation with concomitant reduction in the release of proinflammatory cytokine interleukin-1β (IL-1β). TBHQ has the efficacy of post-injury administration in attenuating acute neurological injury after ICH.Animal Model:Male CD-1 mice (8-10 weeks old)
Dosage:50 mg/kg
Administration:Intraperitoneal injection; three injections at intervals of 8 hours that began 1h post ICH.
Result:The treatment augmented the DNA-binding activity of Nrf2, attenuated brain oxidative damage, attenuated the microglial activation and the expression of IL-1β.
体外研究：
TBHQ (t-butylhydroquinone; tBHQ; 0-100 μM; 48 hours; H9c2 cells) alone does not affect H9c2 cells viability. Pre-incubation of the H9c2 cells with various concentrations of tBHQ for 24 hours enhances cell viability which is decreased due to exposure to ethanol in a dose-dependent manner. Treatment with tBHQ markedly enhances the viability of H9c2 cardiomyocytes exposed to ethanol.TBHQ (5 μM; 15 min; H9c2 cells) treatment significantly reduces the amount of apoptotic cells exposed to ethanol.TBHQ (5 μM; H9c2 cells) pre-treatment markedly inhibites the ethanol-induced increase in caspase-3 and Bax expression, and enhances Bcl-2 expression.
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