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. 2015 Aug 11;5:13005. doi: 10.1038/srep13005

Figure 8. Effects of TBHQ on Akt activation and cell apoptosis in vitro.

Figure 8

(A) Effects of TBHQ treatment at different concentrations for 24 hr on Akt phosphorylation in cultured H9c2 cells. (B) Effects of TBHQ (20 μM), wortmannin (10 nM) and Akt Inhibitor (Akti) (10 μM) pretreatments on Akt phosphorylation and 4-HNE (20 μM for 24 hr)-induced caspase 3 cleavage in H9c2 cells. c-Casp3, cleaved form of caspase 3. (C) Effects of wortmannin and Akt Inhibitor on the basal level of Akt phosphorylation. (D) Effects of TBHQ, wortmannin and Akti on 4-HNE-induced caspase 3/7 activation in H9c2 cells (expressed as arbitrary luminescence intensity). (E) Western blot showing the effects of TBHQ (20 μM for 12 hr) on Akt phosphorylation in the absence or presence of 4-HNE (20 μM) in rat primary cardiac myocytes. (F) Effects of TBHQ on 4-HNE-induced apoptosis in rat primary myocytes as measured by caspase 3/7 activity. (G) Effects of TBHQ on 4-HNE-induced apoptosis in rat primary myocytes in the presence of endothelin-1 (ET-1, 100 nM). *P < 0.05, one-way ANOVA (n = 3–4 independent experiments).