Knockdown of Sestrin2 Increases Lipopolysaccharide-Induced Oxidative Stress, Apoptosis, and Fibrotic Reactions in H9c2 Cells and Heart Tissues of Mice via an AMPK-Dependent Mechanism

Figure 1

Sesn2 knockdown increases LPS-mediated oxidative stress through an AMPK-dependent pathway in H9c2 cells. (a) H9c2 cells were stimulated with various doses of LPS for 6 h. (b) siRNA targeting rat sesn2 was transfected into H9c2 cells, and the level of phosphorylated AMPK was determined by Western blotting. (c and d) Sesn2 knockdown H9c2 cells were incubated with LPS or LPS plus AICAR for 4 h. Western blotting was then used to determine the levels of catalase and SOD2. (e) Sesn2 knockdown cells were stimulated with LPS or LPS plus AICAR for 6 h, after which ROS levels were analyzed by DHE staining (red). All graphs were obtained from three separate experiments. Data are presented as means; error bars represent ±SD (NS: not significant; versus control; ; ; ; ANOVA).

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