TBHQ

TBHQ处理预防了TAC诱导的左室扩张和心脏功能障碍，并降低了心肌细胞凋亡的发生率。TBHQ诱导的Akt激活伴随着Bad、糖原合成酶激酶-3β（GSK-3β）和哺乳动物雷帕霉素靶蛋白（mTOR）的磷酸化增加。体内阻断Akt通路加速了心脏功能障碍，并消除了TBHQ的保护效果。TBHQ还减少了应激心肌中的反应性醛类产物和蛋白质氧化的产生[3]。

HeLa细胞经t2,5-Di-tert-butylhydroquinone处理后，表现出对线粒体硫氧还蛋白-2(Trx2)的优先氧化，而细胞内谷胱甘肽和细胞质硫氧还蛋白-1未受影响。t2,5-Di-tert-butylhydroquinone处理促使Trx2过表达抑制了Nrf2的积累和活性[1]。在用t2,5-Di-tert-butylhydroquinone预处理Jurkat T细胞，并随之用抗CD3/抗CD28激活之前，能显著降低白介素-2(IL-2)在转录和蛋白水平上的产生。同样，CD25的表达也在经t2,5-Di-tert-butylhydroquinone预处理后减少，尽管此减少的程度较IL-2为轻[2]。

DMSO:50 mg/mL (300.81 mM)

Jurkat T cells were cultured in 96-well plates (1×10^5 cells/well) and treated as described, and cell supernatants were harvested 24h after activation with anti-CD3/anti-CD28. IL-2 was quantified from cell supernatants by the use of a commercially available kit per the manufacturer's protocol. Relative light intensity was quantified at 450nm by Bio-Tek μQuant microplate reader. The IL-2 concentrations of each sample were then calculated using a line ar standard curve on Microsoft Excel [2].

TBHQ powder was directly mixed with the animal food powder at a ratio of 1% (w/w) as described previously. The efficacy of this protocol for TBHQ treatment in vivo has also been validated by other groups. TBHQ treatment was continued for 4 weeks after the TAC surgery [3].