TBHQ, known as tert-Butylhydroquinone, is commonly employed as an Nrf2 activator and offers protection from cardiotoxicity caused by Doxorubicin (DOX) by stimulating Nrf2[1]. Additionally, TBHQ serves as an ERK activator and counteracts the inhibitory effect on cell proliferation in melanoma induced by Dehydrocorydaline (DHC)[2]. TBHQ, when used alone at concentrations ranging from 0 to 100 μM over 48 hours, does not compromise the viability of H9c2 cells. However, a 24-hour pre-treatment with TBHQ at varying concentrations significantly bolsters the viability of H9c2 cells, which otherwise diminishes in response to ethanol in a dose-responsive manner. Furthermore, TBHQ treatment notably improves the survival of H9c2 cardiomyocytes challenged with ethanol. Additionally, a brief 15-minute exposure to 5 μM TBHQ substantially curtails the number of apoptotic cells in H9c2 cells subjected to ethanol. Moreover, pre-treating H9c2 cells with 5 μM TBHQ significantly hampers the ethanol-triggered upsurge in caspase-3 and Bax levels, while concurrently elevating Bcl-2 expression[3].
TBHQ/特丁基对苯二酚 动物研究
Animal study
Treatment with TBHQ (50 mg/kg; intraperitoneal injection; three injections at 8-hour intervals starting 1 hour after ICH; in CD-1 mice) enhances Nrf2's DNA-binding activity, reduces oxidative damage to the brain and acute neurological deficits following intracerebral hemorrhage (ICH), and diminishes microglial activation, which is associated with a decrease in the release of the proinflammatory cytokine interleukin-1β (IL-1β). TBHQ demonstrates effectiveness in post-injury treatment for mitigating acute neurological damage post-ICH[4].
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