Cucurbitacin I Protects H9c2 Cardiomyoblasts against H₂O₂-Induced Oxidative Stress via Protection of Mitochondrial Dysfunction

Figure 5

Cu I blocks the activation of MAPK signaling pathway in H₂O₂-treated H9c2 cardiomyoblasts. Western blot analysis of the protein expression levels of the total and phosphorylated forms of ERK1/2, JNK, and p38 in H9c2 cardiomyocytes (a) treated with Cu I for 48 h or (c) pretreated with 0.1, 0.5, and 1 μM Cu I for 24 h followed by exposure to 500 μM H₂O₂ for additional 24 h. (b, d) The protein expression levels were quantified by scanning densitometry. β-Actin was used as the loading control. Western blot analysis was performed in triplicate with three independent samples. Data are expressed as fold changes ± SEM versus control cells. Significance was analyzed using a one-way ANOVA followed by the Bonferroni post hoc test. and versus control cells. , , and versus H₂O₂ alone-treated cells. Cont: control; Cu I: cucurbitacin I.

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