[miR-27a induces ferroptosis by inhibiting solute carrier family 7 member-11 (SLC7A11) and causes cerebral ischemia-reperfusion injury in rats].

Objective To investigate the role and molecular mechanism of miR-27a in cerebral ischemia reperfusion injury model in rats. Methods The male Sprague Dawley rats were randomly divided into control group, sham group, middle cerebral artery occlusion/reperfusion model group(MCAO/R group)( according to different ischemia reperfusion time, the model group was divided into the 3, 6, 12 and 24 hours reperfusion groups after 2 hour-ischemia), and vehicle group, agomir-27a group, antagomir-27a group. The Zea-Longa method was used to establish rat MCAO model. The levels of miR-27a and solute carrier family 7 member-11 (SLC7A11) in brain tissues were detected by real-time fluorescence quantitative PCR. Zea-Longa score was used to evaluate neuro score. 2, 3, 5 triphenyl tetrazolium chloride(TTC) staining was used to test the infarct volume. The relative expression levels of glutathione peroxidase 4(GPx4) and SLC7A11 proteins were detected by Western blot analysis. The contents of GSH, Fe and MDA were detected by GSH, Fe and MDA detection kits. The target gene of miR-27a was confirmed by dual luciferase reporter gene technique. Results After cerebral ischemia reperfusion, the level of miR-27a was up-regulated and the level of SLC7A11 was down-regulated. Inhibition of miR-27a expression reduced neurological score and cerebral infarct volume, and inhibited ferroptosis after cerebral ischemia reperfusion. Conclusion In the process of cerebral ischemia and reperfusion, the up-regulated miR-27a may induce ferroptosis through inhibiting SLC7A11, thus causing brain tissue damage.