The Protection Of LncRNA SNHG8 On Hypoxia-reoxygenation H9C2 Cell Injury

Aim: Extensive research has been conducted on the effect of long non-coding RNAs(lncRNAs)in a variety of diseases,including cancers and acute myocardial infarction(AMI).This study aimed to investigate the protective role of lncRNA SNHG8 in hypoxia-ischemia-reoxygenation(HI/R)-induced myocardial injury and its potential mechanism of action.Methods: Cell viability,proliferation,CK-MB,cell apoptosis and protein expression were determined by CCK-8 assay,Ed U assay,ELISA,flow cytometry and western blot.The relationship between SNHG8 and miR-335 was confirmed by a dual luciferase reporter gene assay.Results: Gene microarray screening of a series of lncRNAs in HI/R-induced H9C2 cells,showing that TUG1,SNHG8 and Fox O3-AS1 were highly expressed in HI/ R-induced H9C2 cells,and SNHG8 was highest.Then,we further determined the protective effect of SNHG8 in HI/R-induced H9C2 cells through CCK-8 cell activity test,EDU proliferation test and apoptosis test.The results showed that interference of SNHG8 si RNA could significantly increase the HI/R-induced H9C2 cell viability and proliferation,it also could significantly down-regulate HI/R induced H9C2 apoptosis.Next,we screened the expression of some miRNAs in HI/R-induced H9C2 cardiomyocytes,and then combined with Star Base analysis,showing that a relationship between SNHG8 and miR-335,which also has been confirmed by dual luciferase reporter assay.Further experiments confirmed that transfection of SNHG8 si RNA could reverse the effects of miR-335 inhibitor on increasing apoptosis and decreasing cell viability.We used Targetscan(http://www.targetscan.org/)and miRTar Base m RNA to explore the binding sites of miR-335,the results showed that the overlapping analysis of 196 differentially expressed m RNAs predicted by Target Scan and 1 m RNA predicted by miRTar Base showed that only RASA1 interacted with miR-335.Furthermore,we found that miR-335 could regulate RASA1 expression and transfected with SNHG8 si RNA could down-regulate RASA1 expression.Silencing of RASA1 protected against HI/R-induced H9C2 cell injury.However,SNHG8 did not further reduce apoptosis,further demonstrating that SNHG8 acts through RASA1 and RASA1 mediated the protection of SNHG8 on HI/R myocardial injury.Conclusions: Taken together,lncRNASNHG8 alleviated HI/R-induced myocardial damage by regulating miR-335 and RASA1.