TBHQ

Research use only, not for human use.

Tert-butylhydroquinone (tBHQ) is an antioxidant that induces an antioxidant response through the redox-sensitive transcription factor Nrf2.

Tert-butylhydroquinone (tBHQ) is an antioxidant that induces an antioxidant response through the redox-sensitive transcription factor Nrf2.(In Vitro):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.(In Vivo):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.

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. Cell Viability Assay Cell Line:H9c2 cells Concentration:0 μM, 0.625 μM, 1.25 μM, 2.5 μM, 5 μM, 10 μM, 20 μM, 50 μM and 100 μM Incubation Time:48 hours Result:Enhanced the viability of H9c2 cardiomyocytes exposed to ethanol.Apoptosis Analysis Cell Line:H9c2 cells Concentration:5 μM Incubation Time:Result:Lowered the amount of apoptotic cells exposed to ethanol.Western Blot Analysis Cell Line:H9c2 cells Concentration:5 μM Incubation Time:Result:Inhibited the ethanol-induced increase in caspase-3 and Bax expression, and enhanced Bcl-2 expression.

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.

tert-Butylhydroquinone

Nuclear Receptor/Transcription Factor

Keap1-Nrf2

Nrf2

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1948-33-0

166.22

C10H14O2

>98% (HPLC)

DMSO: 30 mg/mL (180.48 mM)

CC(C)(C)c1cc(O)ccc1O

2-(tert-butyl)benzene-14-diol

(-20℃)

With Ice Pack

≥ 2 years