MiR320 Inhibits Vascular Endothelial Cell Pyroptosis Via Improving Mitochondrial Function

[Objective] To observe the effect of miR320 on endothelial cell pyroptosis and explore its potential mechanism.[Methods](1)MiR320 inhibitor was transfected into vascular endothelial cells for 48 h,and the effects of miR320 inhibitor on mitochondrial morphology,ATP production,membrane potential,ROS content and pyroptosis related protein of vascular endothelial cells were observed.(2)miR320 mimic transfected vascular endothelial cells for 48 h,the effects of miR320 mimic on mitochondrial morphology,ATP production,membrane potential,ROS content and pyproptosis related protein were observed.(3)ROS scavenger NAC was used to observe the effects of ROS on vascular endothelial cells pyroptosis induced by miR320 inhibitor.[Results] Mitochondrial numbers in MiR320 inhibitor-treated vascular endothelial cells were increased,and mitochondrial DRP1 protein expression was increased,but BNIP3 expression was significantly down-regulated.There was no significant change in mitochondrial membrane potential.However,the ATP production was decreased and intracellular ROS content increased.Moreover,the pyroptosis related protein NLRP3,GSDMD,Caspase 1,IL-18,and IL-1? were significantly up-regulated.Mitochondrial numbers in MiR320 minic-treated vascular endothelial cells were decreased.Mitochondrial DRP1 protein expression was significantly decreased.The BNIP3 expression was significantly up-regulated.The mitochondrial membrane potential was no significant changed.However,the ATP content was obviously increased and intracellular ROS content was significantly decreased.Moreover,the pyroptosis related protein NLRP3,GSDMD,Caspase 1,IL-18,and IL-1? were significantly down-regulated.The ROS scavenger NAC decreased the ROS content and up-regulated the expression of BNIP3,and down-regulated the expression of NLRP3,GSDMD,IL-1?,and IL-18 in vascular endothelial cells induced with miR320 inhibitor.[Conclusion] miR320 improves mitochondrial function and inhibits ROS-mediated vascular endothelial cell pyroptosis.