Protective Effect of Sodium Hydrosulfide on Lipopolysaccharide Induced Myocardial Cell Injury Model: Involvement of Oxidative Stress and Endoplasmic Reticulum Stress

Lipopolysaccharide can induce myocardial cell injury, which has been widely used in the preparation of septic cardiomyopathy models. We herein aimed to evaluate protective effects sodium hydrosulfide against oxidative stress and endoplasmic reticulum on model explore whether protein kinase RNA-like kinase-eukaryotic initiation factor 2 alpha signaling pathways was involved. The sepsis induced established by inducing rat cardiomyoblast line H9c2 cells with lipopolysaccharide endogenous hydrogen sulfide inhibitor (DL-propargylglycine) were for intervention treatment. Then, viability, levels, lactate dehydrogenase, reactive oxygen species, superoxide dismutase, glutathione malondialdehyde determined using commercial assay kits; enzyme-linked immunosorbent determine creatine kinase-myoglobin binding, interleukin-6, tumor necrosis interleukin-10; reverse transcription-polymerase chain reaction cystathionine gamma-lyase messenger RNA expression; Western blot glucose-regulated 78, kinase, phosphorylated eukaryotic alpha, activating transcription 4 C/EBP-homologous levels. Sodium increased contents cells, but did not affect expression gamma-lyase. It attenuated decrease viability caused lipopolysaccharide; reduced release enzymes like dehydrogenase binding; level inflammatory factors interleukin-6 alpha; stress; inhibited pathway proteins. treatment improves inhibiting via kinaseeukaryotic pathway, may be a theory cardiomyopathy.