Atorvastatin and Long Noncoding RNA MEG3 Exhibit Protective Effect on Brain Injury Induced by Subarachnoid Hemorrhage via Sponging miR-145-5p

Abstract

The present study investigated the effect of atorvastatin and Long noncoding RNA MEG3 on
brain injury induced by subarachnoid hemorrhage in vivo. In SAH animal model brain water content analysis was used to calculate percentage of water in brains. Expressions of LncRNA MEG3 as well as miR-145-5p
were measured with RT-qPCR. Cell viabilities of nerve cells were detected by CCK-8. Flow cytometry was
for examining apoptosis rate. Dual luciferase reporter assay verified the binding between MEG3 and miR145-5p. Proteins of apoptosis or inflammation biomarkers were evaluated through western blot. LncRNA
MEG3 expressions were increased in SAH rat nerve cells with time growing. SAH could reduce cell viabilities and increase apoptosis as well as inflammation. Knockdown of LncNRA MEG3 could upregulate viabilities of nerve cells after SAH and inhibit apoptosis and inflammation. MiR-145-5p was a target of LncRNA
MEG3. The miR-145-5p could enhance viabilities and suppress apoptosis and inflammation factors IL-1β
and TNF-α. Atorvastatin could downregulate brain water content and improve cell viabilities and repress
apoptosis and inflammation. The miR-145-5p and atorvastatin showed negative correlation with LncRNA
MEG3. Moreover, miR-145-5p and atorvastatin had positive correlation in detecting cell viabilities, apoptosis and inflammation. MiR-145-5p and atorvastatin could reverse functions of LncRNA MEG3 in SAH nerve
cells as protector.