Metformin Protects H9C2 Cardiomyocytes from High-Glucose and Hypoxia/Reoxygenation Injury via Inhibition of Reactive Oxygen Species Generation and Inflammatory Responses: Role of AMPK and JNK

Figure 2

AMPK pathway was inhibited during H/R injury and exacerbated by HG and the cytoprotective effects of metformin were dependent on AMPK activation. H9C2 cells were treated with HG (33 mM), H/R, and HG + H/R. The expression of P-AMPK, T-AMPK (a) and P-ACC, T-ACC (b) was measured by Western blots. (c) Expression of P-AMPK and T-AMPK in the H9C2 cells treated with different concentrations of metformin (0, 1, 5, and 10 mM) was measured by Western blots. (d) Cells were treated with HG + H/R, metformin (5 mM) + HG + H/R, compound C (1 μM), or metformin + HG + H/R + compound C. Cell viability of each group was established using the CCK-8 assay. versus control; versus HG or H/R; versus metformin + HG + H/R. Data are shown as means ± SD of 3 independent experiments.

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