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. Author manuscript; available in PMC: 2012 Aug 10.
Published in final edited form as: Arch Pharm Res. 2012 Aug 3;35(7):1259–1267. doi: 10.1007/s12272-012-0717-3

Fig. 6.

Fig. 6

Effect of gRb1 on phosphorylation of JNK in H2O2-exposed cardiomyocytes. The cells were pretreated with gRb1 (1 μM) or gRb1/SP600125 (SP, 10 μM) for 2 h prior to the H2O2 and concurrent treated with H2O2 (0.5 mM) for 2 h. The phosphorylation of JNK (p-JNK) was analyzed by western blots. Upper panel: Representative immunoblots of p-JNK in cardiomyocytes. The gRb1 attenuated the increased p-JNK caused by H2O2 (#p < 0.01) that was further attenuated by a JNK inhibitor SP (10 μM), &p < 0.05 vs gRb1/H2O2-treated cells. gRb1 and SP treatment alone had no effect on p-JNK. Lower panel: Densitometry showing the mean ± S.E.M. of four experiments for each condition. α-tubulin: a loading control.