Aucubin Protects against Myocardial Infarction-Induced Cardiac Remodeling via nNOS/NO-Regulated Oxidative Stress

Figure 4

Aucubin inhibits MI and hypoxia-induced activation of the TNFα-ASK1-JNK signal. (a) and (b) Western blot analysis of TNFα, phosphorylated (p-) and total ASK1, and JNK in the indicated mouse hearts post-MI ((a) representative blots and (b) statistical analysis result) (, versus vehicle-sham and versus vehicle-MI). (c) and (d) Western blot analysis of TNFα, phosphorylated (p-) and total ASK1, and JNK in the aucubin- (10 μM, 50 μM) pretreated H9c2 cardiomyocytes after exposure to hypoxia for 24 h ((c) representative blots and (d) statistical analysis result) ( sample). versus normoxia + PBS and versus hypoxia + PBS (e–h). H9c2 cardiomyocytes were pretreated with a JNK inhibitor, SP600125 (10 μM), or JNK agonist, anisomycin (40 ng/ml), and/or aucubin (50 μM) for 12 h and then exposed to hypoxia for 24 h. (e) and (g) TUNEL staining and quantitation in the indicated group ( sample). (f) and (h) Representative Western blots and quantitation of c-caspase 3 in the indicated group ( sample). versus normoxia + PBS and versus hypoxia + PBS. All experiments were repeated independently three times.

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