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 3

Metformin attenuated HG + H/R induced decrease in cell viability by preservation of mitochondrial membrane integrity and mitigating oxidative stress. H9C2 cells were treated with HG + H/R, metformin (5 mM), metformin + HG + H/R, compound C (1 μM), and metformin + HG + H/R + compound C. (a) Mitochondrial membrane potential evidenced by JC-1 staining. (b) ROS generation was measured by the DCF fluorescence intensity. (c) Bars represent quantified ROS generation. (d) Mitochondrial electron transport chain complex I and complex III activities were measured with commercial kits. versus control; versus HG + H/R; versus metformin + HG + H/R. Data in the bar graphs are calculated as means ± SD of 3 independent experiments.

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