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

Figure 1

Cytotoxicity of Cu I in H9c2 cardiomyoblasts. Cell viability was measured using the MTT assay in cells treated with 0.1, 0.5, and 1 μM for (a) 24 h or (b) 48 h. (c) Representative images and (d) fluorescence intensities of DCFH-DA staining assay in cells treated with 0.1, 0.5, and 1 μM Cu I for 48 h. (e) Western blot analysis of SOD-1, catalase, and GPx protein expression levels in cells treated with Cu I for 48 h. (g) Representative images of TUNEL staining assay in cells pretreated with Cu I for 48 h. (h) Western blot analysis of Bax and Bcl-2 protein expression levels in Cu I-treated cells for 48 h. (f, i) 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 the % changes ± SEM versus control cells from three independent experiments. Significance was analyzed by a one-way ANOVA followed by the Bonferroni post hoc test. Cont: control; Cu I: cucurbitacin I; NS: not significant. Scale bar: 100 μm.

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