Role And Mechanism Of The LncRNA SNHG1/miR-450b-5p/IGF1 Axis In The Regulation Of Myocardial Ischemia Reperfusion Injury

Purpose:The pathogenesis of myocardial ischemia-reperfusion injury(MIRI)is complex and involves many physiological and biochemical processes.Non-coding Rnas play an important role,including several lnc RNA and microRNA that have been reported.This study aims to explore the related mechanism of LncRNA SNHG1/ Mir-450B-5P/IGF1 axis in myocardial ischemia-reperfusion injury,and it is of great significance to find effective targets and methods for alleviating or alleviating myocardial ischemia-reperfusion injury.MethodsAfter hypoxia/reoxygenation(H/R)induction,the expression levels of LncRNA SNHG1 were detected using reverse transcription-quantitative PCR.After overexpression of LncRNA SNHG1 by cell transfection,cell viability was detected using an MTT assay,the apoptotic rates were detected using TUNEL staining,apoptosis-related protein expression levels were detected using western blotting and respective kits were used to measure the oxidative stress levels.The ENCORI database predicted the presence of binding sites between LncRNA SNHG1 with miR-450b-5p,and between microRNA(miR)-450b-5p and insulin-like growth factor1(IGF1),and this was verified using luciferase reporter assays.Next,the regulatory mechanism of LncRNA SNHG1/miR-450b-5p/IGF1 in MIRI was explored by overexpression of miR-450b-5p and downregulation of IGF1 expression in H/R-induced cells.Finally,the expression of the PI3K/Akt signaling pathway members were detected using western blotting.LncRNA SNHG1 expression was downregulated in H/R-induced AC16 cells.Results:Overexpression of LncRNA SNHG1 inhibited H/R-induced apoptosis of AC16 cells and reduced the oxidative stress levels in AC16 cells induced by H/R,which was mediated via regulation of a miR-450b-5p/IGF1 axis and the activation of PI3K/Akt signaling pathway.The activation of the PI3K/Akt pathway by the LncRNA SNHG1/miR-450b-5p/IGF1 axis inhibited the apoptosis and oxidative stress levels of AC16 cells induced by H/R.Conclusion:Overexpression of LncRNA SNHG1 can protect H/R cells and I/R animal models from reperfusion injury.In addition,this study suggested that activation of PI3K/Akt signaling pathway by lnc RNA SNHG1/ Mir-450B-5p /IGF1 axis inhibits cell apoptosis and oxidative stress induced by H/R.