Abstract

To explore the protective mechanism of total flavonoids from Eucommia ulmoides Oliver leaves (thin-film electroluminescent) on lipopolysaccharide-induced cardiomyocyte H9C2 injury. Cardiomyocytes were divided into control, lipopolysaccharides, lipopolysaccharides+thin-film electroluminescent-low group, lipopolysaccharides+thin-film electroluminescent-middle, lipopolysaccharides+thin-film electroluminescent-high, lipopolysaccharides+microRNA-negative control, lipopolysaccharides+microRNA-494, lipopolysaccharides+thin-film electroluminescent+anti-microRNA-negative control, and lipopolysaccharides+thin-film electroluminescent+anti-microRNA-494 groups. The commercial kits were used to evaluate superoxide dismutase and glutathione peroxidase activities, as well as malondialdehyde levels. Flow cytometry was utilized for the estimation of cell apoptosis. Western blotting was employed to detect cleaved caspase-3 and cleaved caspase-9 protein levels. Reverse transcription-quantitative polymerase chain reaction was selected to detect microRNA-494 expression. Lipopolysaccharides significantly decreased malondialdehyde levels, increased glutathione peroxidase and superoxide dismutase activities, induced cell apoptosis, and upregulated cleaved caspase-3 and cleaved caspase-9 protein levels in cardiomyocytes, suggesting that lipopolysaccharides facilitated cardiomyocyte oxidative stress and apoptosis. Thin-film electroluminescent overtly weakened lipopolysaccharides induced cardiomyocyte oxidative stress and apoptosis in a dose-dependent mode. Thin-film electroluminescent partly overturned lipopolysaccharides induced downregulation of microRNA-494 expression in cardiomyocytes. Furthermore, elevation of microRNA-494 impaired lipopolysaccharides-induced cardiomyocyte oxidative stress and apoptosis. In addition, microRNA-494 knockdown weakened thin-film electroluminescent mediated repressive effects on lipopolysaccharides induced cardiomyocyte oxidative stress and apoptosis. Thin-film electroluminescent could alleviate lipopolysaccharides induced cardiomyocyte oxidative stress and apoptosis, which was achieved by upregulating microRNA-494 expression.