Abstract

This work was performed to analyze the effect of polysaccharides from semen plantaginis on myocardial cell hypoxia/reoxygenation injury as well as its molecular mechanism. Rat myocardial cells H9C2 were exposed to various concentrations of plantaginis and then subjected to transfection and/or plantaginis treatment, dividing into control, hypoxia/reoxygenation, hypoxia/reoxygenation+L-plantaginis, hypoxia/reoxygenation+M-plantaginis, hypoxia/reoxygenation+H-plantaginis, hypoxia/reoxygenation+si-circTTC3, hypoxia/reoxygenation+si-negative control, and hypoxia/reoxygenation+plantaginis+plasmid cloning deoxyribonucleic acid-circTTC3 groups. Cell viability was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyl tetrazolium bromide assay. Flow cytometry, Western blotting as well as enzyme-linked immunosorbent assays were used to analyze cell apoptosis or oxidative stress. CircTTC3 and microRNA-27a-3p levels were detected by real-time quantitative polymerase chain reaction. The targeting relationship between circTTC3 and microRNA-27a-3p was examined by dual-luciferase reporter assay. Treatment with different concentrations of plantaginis increased hypoxia/reoxygenation induced H9C2 cell viability and superoxide dismutase activity but decreased apoptosis rate, cleaved caspase-3 expression levels, malondialdehyde content, and lactate dehydrogenase activity in a concentration-dependent manner, accompanied by a decrease of circTTC3 expression and increase of microRNA-27a-3p expression (p<0.05). CircTTC3 targeted microRNA-27a-3p, and inhibition of circTTC3 expression increased myocardial cell viability and superoxide dismutase activity and decreased apoptosis rate, cleaved caspase-3 expression levels, malondialdehyde content and lactate dehydrogenase activity (p<0.05). Overexpression of circTTC3 reversed the effect of plantaginis on hypoxia/reoxygenation caused myocardial cell damage. Plantaginis regulates circTTC3/microRNA-27a-3p axis to attenuate myocardial cell hypoxia/reoxygenation injury.