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. 2015 Nov 16;5:16590. doi: 10.1038/srep16590

Figure 4. The role of ERK1/2 and PI3 K/Akt pathway in CST’s protective effects during A/R in cardiomyoblasts.

Figure 4

H9c2 cardiomyoblasts were pretreated with ERK inhibitor PD98059 (20 μM), PI3 K/Akt inhibitor wortmannin (10 nM) for 30 min, followed by treatment with CST (100 nM) for 30 min, then cells underwent A/R. (a) Apoptosis was assessed by cleaved caspase-3–positive cells (a) and counted (b). Scale bars = 50 μM. Western blot analysis of ER stress-markers expression(c), and relative protein expression was analyzed (d). Six independent experiments were performed for above studies. (e) Western blot analyzed the changes of phosphorylated ERK1/2, Akt and eNOS during CP in isolated heart; and expressions analysis (f) was showed. Three independent experiments were done for it.