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. 2018 Dec 1;11(12):5840–5849.

Figure 3.

Figure 3

Melatonin treatment ameliorated hypoxic injury by reducing cardiomyocyte apoptosis, and activating PI3K/Akt signaling, while these protective effects were attenuated by LY294002 treatment. H9C2 cardiac cells were treated with LY294002 (20 μM) for 1 h prior to stimulation with melatonin, followed by 48 h hypoxia treatment. A. Effects of melatonin on cell viability determined by CCK-8 in cultured H9C2 cells. B. Representative western blot of phosphorylation of PI3K and Akt in different groups with or without LY294002. C. Ratio of phosphorylated PI3K/ total PI3K. D. Ratio of phosphorylated Akt/total Akt. E. Representative western blotting of Bcl2, Bax, and cleaved Caspase 3. β-actin was used as the internal control. F-H. The relative levels of Bcl2, Bax, and cleaved Caspase 3. The results are expressed as the means ± SEM, n=3. *P<0.05 versus control group, #p<0.05 versus hypoxia group, &P<0.05 versus hypoxia + melatonin group.