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MedChemExpress - Model TBHQ - 1948-33-0

MedChemExpress - Model TBHQ - 1948-33-0

TBHQ (tert-Butylhydroquinone) is a widely used Nrf2 activator, protects against Doxorubicin (DOX)-induced cardiotoxicity through activation of Nrf2[1]. TBHQ (tert-Butylhydroquinone) is also an ERK activator; rescues Dehydrocorydaline (DHC)-induced cell proliferation inhibitionin melanoma[2].

TBHQ

MCE China：TBHQ

Brand：MedChemExpress (MCE)

Cat. No.HY-100489

CAS：1948-33-0

Synonyms：tert-Butylhydroquinone

Purity：99.89%

Storage：Store at room temperature 3 years In solvent -80°C 2 years -20°C 1 year

Shipping：Room temperature in continental US; may vary elsewhere.

Description：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.

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[3]. TBHQ (5 μM; 15 min; H9c2 cells) treatment significantly reduces the amount of apoptotic cells exposed to ethanol[3]. TBHQ (5 μM; H9c2 cells) pre-treatment markedly inhibites the ethanol-induced increase in caspase-3 and Bax expression, and enhances Bcl-2 expression[3].

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[4].

IC50 & Target：Nrf2 ERK Autophagy

References：

[1]. Lin-Feng Wang, et al. Tert-butylhydroquinone ameliorates doxorubicin-induced cardiotoxicity by activating Nrf2 and inducing the expression of its target genes. Am J Transl Res. 2015; 7(10): 1724–1735. [Content Brief]

[2]. XIAOJING SHI, et al. Tert-butylhydroquinone attenuates the ethanol-induced apoptosis of and activates the Nrf2 antioxidant defense pathway in H9c2 cardiomyocytes.Int J Mol Med. 2016 Jul; 38(1): 123–130. [Content Brief]

[3]. Hu H, et al. Dehydrocorydaline inhibits cell proliferation, migration and invasion via suppressing MEK1/2-ERK1/2 cascade in melanoma.Onco Targets Ther. 2019 Jul 2;12:5163-5175. [Content Brief]

[4]. Sukumari-Ramesh S, et al. Post-Injury Administration of Tert-butylhydroquinone Attenuates Acute Neurological Injury AfterIntracerebral Hemorrhage in Mice.J Mol Neurosci. 2016 Apr;58(4):525-31. [Content Brief]

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