TBHQ


CAS No. : 1948-33-0

(Synonyms: tert-Butylhydroquinone)

1948-33-0
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Cat. No. : HY-100489
M.Wt: 166.22
Formula: C10H14O2
Purity: >98 %
Solubility: DMSO : ≥ 56.66 mg/mL (340.87 mM)
Introduction of 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]. 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].

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