Abstract:To explore the effects of astragalus polysaccharide combined with long non-coding RNA (lncRNA) and taurine up-regulated gene 1 (TUG1) on the apoptosis of human cardiac microvascular endothelial cells after ischemia-reperfusion.Methods:Cardiac microvascular endothelial cells were divided into a control group,a model group,sh-NC group,sh-TUG1 group,astragalus polysaccharide group,astragalus polysaccharide+sh-TUG1 group.Flow cytometry was used to detect apoptosis,and Western Blotting method was used to detect sonic hedgehog (SHH) expression.ELISA method to detect tumor necrosis factor-α (TNF-α) content,and DCFH-DA method was used to detect reactive oxygen species (ROS) content.Results:Compared with the control group,cardiac microvascular endothelial cells in the model group apoptosis rate increased,TNF-αincreased,ROS content increased,SHH protein expression decreased (Ps<0.05); compared with sh-NC group,cardiac microvascular endothelial cells of sh-TUG1 group apoptosis rate decreased,TNF-α decreased,ROS decreased,SHH protein expression increased (all Ps<0.05); compared with the model group,the apoptosis rate of cardiac microvascular endothelial cells in the astragalus polysaccharide group decreased,TNF-α decreased,ROS decreased,SHH protein expression increased (all Ps<0.05); compared with the sh-TUG1 and the astragalus polysaccharide group,the apoptosis rate of cardiac microvascular endothelial cells in the astragalus polysaccharide+sh-TUG1 group decreased,TNF-α decreased,ROS decreased,SHH protein expression increased (Ps<0.05).Conclusion:Astragalus polysaccharide combined with TUG1 gene silencing can reduce the apoptosis of ischemia-reperfusion human cardiac microvascular endothelial cells,reduce oxidative damage,and inhibit the secretion of inflammatory factors,the mechanism may be related to the activation of SHH signaling pathway.