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 4

Sesn2 knockdown increases LPS-mediated cell death signaling in C57BL/6 mice. (a) To assess sens2 knockdown efficiency in heart tissue, Western blotting was used to measure the protein levels of sesn2 and phosphorylated AMPK. (b) The levels of catalase and SOD2 were determined by Western blotting. (c) The activities of catalase and SOD were measured using commercial assay kit. (d) The ratio of Bax to Bcl-xL was detected by Western blotting. (e) Caspase-3 activity in heart tissue was measured using a Caspase-3 Activity Assay Kit. All graphs present data from four mice per group (C: control mice; L: LPS only-treated mice; LS: sesn2 siRNA plus LPS-treated mice; LSA: sesn2 siRNA plus LPS and AICAR-treated mice). Data are presented as means; error bars represent ±SD (; ; ANOVA).

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