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Objective. Myocardial infarction (MI) is a serious heart health problem in the world with a high mortality rate. Our study is mainly aimed at validating the antioxidative stress and antiapoptotic effects of escin in a H2O2-induced cardiomyocyte injury model. Methods. H9c2 cells were divided into control group, H2O2 treatment group, and H2O2+escin group. We studied the effect of escin on H9c2 cells and its mechanism by flow cytometry, real-time PCR, CCK-8 assay and Western blot. Cell morphology was observed by cell staining and optical microscopy. Results. We found that the level of reactive oxygen species (ROS) in the H2O2 treatment group was significantly elevated, while the high level of ROS was significantly reversed after treatment with escin. The protein levels of SOD1, SOD2, Bcl-2, and IκB-α in the H2O2 treatment group were significantly decreased compared with the H2O2+escin group, and the Bax, TNF-α, IL-1β, p65, and IκKα protein expressions were greatly higher than those in the H2O2+escin group. And the results of PCR were also consistent with those. TUNEL-positive cells also decreased significantly when treated with escin. Flow cytometry showed that the percentage of apoptotic cells decreased greatly after treatment of escin. Through IL-1β immunofluorescence, the fluorescence intensity of the H2O2 treatment group was greatly higher compared with that of the control group, but escin reversed this effect. Conclusions. These results indicated that escin inhibits H2O2-induced H9c2 cell apoptosis, oxidative stress, and inflammatory responses via the NF-κB signaling pathway.

Effects of Escin on Oxidative Stress and Apoptosis of H9c2 Cells Induced by H2O2