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 细胞实验
Cell Line
Concentration
Treated Time
Description
References
Human intestinal epithelial cells (HIEC)
10 μM
48 h
TBHQ significantly decreased LDH release and cell death in 5-FU-treated HIECs and improved their proliferative ability.
Cell Mol Biol Lett. 2021 Nov 18;26(1):48.
L02 cells
10 μM
24 h
tBHQ pretreatment significantly increased Nrf2 expression, inhibited EC-induced lipid peroxidation, and restored GSH levels, indicating that tBHQ suppressed EC-induced ferroptosis by activating the Nrf2 pathway.
Redox Biol. 2022 Jul;53:102349.
Human primary small airway epithelial cells (SAE)
25 µM
15 h
TBHQ treatment resulted in a significant increase in CSE enzymatic activity and CSE mRNA levels
Antioxidants (Basel). 2022 Aug 16;11(8):1582.
Human primary small airway epithelial cells (SAE)
25 µM
15 h
TBHQ treatment led to a significant increase in CSE enzymatic activity and mRNA levels, with a 400% increase in activity and a 10-12-fold increase in mRNA levels.
Antioxidants (Basel). 2022 Aug 16;11(8):1582.
HCT116 cells
5 μM
24 h
TBHQ significantly reversed the downregulation of GPX4 and NQO1 caused by PRDX1 silencing, indicating that NRF2 plays a critical role in suppressing ferroptosis induced by PRDX1 knockdown.
Int J Biol Sci. 2024 Sep 23;20(13):5070-5086.
SW620 cells
5 μM
24 h
TBHQ significantly reversed the downregulation of GPX4 and NQO1 caused by PRDX1 silencing, indicating that NRF2 plays a critical role in suppressing ferroptosis induced by PRDX1 knockdown.
Int J Biol Sci. 2024 Sep 23;20(13):5070-5086.
Hep3B cells
60 μM
8 h
TBHQ increased CUL4A mRNA levels, while WDR23, DDB1, and RBX1 mRNA levels remained unchanged.
J Biol Chem. 2021 Jan-Jun;296:100704.
TBHQ/特丁基对苯二酚 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
C57/BL6 mice
5-FU-induced intestinal mucositis model
Intraperitoneal injection
10 mg/kg
Once daily for 8 days
TBHQ significantly attenuated 5-FU-induced intestinal mucositis in mice, reducing weight loss, diarrhea score, and increasing colon length.
Cell Mol Biol Lett. 2021 Nov 18;26(1):48.
Balb/c mice
EC-induced liver injury model
Intraperitoneal injection
20 mg/kg
Once daily for 21 days
TBHQ pretreatment significantly improved EC-induced liver injury and inflammation, restored Nrf2 expression, and inhibited ferroptosis-related markers, indicating that tBHQ suppressed EC-induced hepatic ferroptosis by activating the Nrf2 pathway.
Redox Biol. 2022 Jul;53:102349.
Mice
CaOx nephrocalcinosis model
Intraperitoneal injection
10 mg/kg
3 days pretreatment followed by 7 days maintenance
To investigate the effect of TBHQ on CaOx-induced kidney injury and crystal deposition, TBHQ partially reversed kidney injury and crystal deposition.
Adv Sci (Weinh). 2024 Dec;11(48):e2408945
Mice
CaOx nephrocalcinosis model
Intraperitoneal injection
75, 100, 125 mg/kg
Once daily for 7 days
To evaluate the effect of ferroptosis inhibition on CaOx-induced kidney injury, it was found that the ferroptosis inhibitor Fer reduced CaOx-induced crystal deposition and kidney injury.
Adv Sci (Weinh). 2024 Dec;11(48):e2408945
Mice
CT26PRDX1-KD xenograft model
Intraperitoneal injection
10 mg/kg
Daily until the end of the experiment
TBHQ significantly restored the expression of NRF2 and GPX4 in the CT26PRDX1-KD group and reversed the inhibitory effect of PRDX1 knockdown on tumor growth, indicating that NRF2 activation suppresses ferroptosis induced by PRDX1 knockdown in vivo.
Int J Biol Sci. 2024 Sep 23;20(13):5070-5086.
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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