Ginsenoside RK3 Prevents Hypoxia-Reoxygenation Induced Apoptosis in H9c2 Cardiomyocytes via AKT and MAPK Pathway

Figure 9

Involvement of ERK1/2, p38, JNK, and RK3 in H/R-induced caspase-3 activation and cytotoxicity. H9c2 cardiomyocytes were pretreated with or without RK3 (25 μg/mL) for 12 h prior to H/R exposure. The expression levels of phosphorylated and total ERK1/2, p38, and JNK were detected by immunoblotting assay (a). The effects of the PD98059 (an ERK1/2-specific inhibitor), SB203580 (a p38-specific inhibitor), and SP600125 (a JNK-specific inhibitor) on caspase-3 activation (b and c) and cell viability (d) were determined. The results are represented as means ± SD from three independent experiments. ^#𝑃<0.05 versus control group; *𝑃<0.05 versus H/R-treated cells; ^$𝑃<0.05 versus H/R+RK3-treated cells.

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