Sevoflurane Preconditioning Regulates The Effects Of MiR-532-5p/PEG3 On Neuroinflammation And Apoptosis During Spinal Cord Ischemia/reperfusion Injury In Rats

Objective: Spinal Cord ischemia/reperfusion injury(SCIRI)is a serious complication of thoracic and abdominal surgery,which can cause loss of sensation and movement,and can cause paraplegia in severe cases.The mechanism of SCIRI is very complex and closely related,mainly including oxidative stress,inflammatory response,autophagy and apoptosis,calcium overload,ferroptosis,and so on.In recent years,a growing number of mi RNAs have been focused on the nerve protection and direction of ischemia-reperfusion injury,including mi R-532-5p high attention;paternally expressed gene 3(PEG3),which resides in the nucleus of brain neurons,has been shown to be associated with myocardial ischemia-reperfusion injury.Sevoflurane preconditioning has been validated to be organ-protection.This study aims to explore the effect of sevoflurane preconditioning on SCIRI by regulating mi R-532-5p,and then targeting PEG3.Methods: Sevoflurane preconditioning can improve neuromotor function scores,reduce BSCB permeability,and increase the number of surviving motoneurons in the anterior horn of the spinal cord.Compared with Sham,mir-523-5p expression in the IR group decreased at 24 h,and PEG3 expression increased.PEG3 is the target protein of mi R-532-5p,and mi R-532-5p can inhibit the expression of PEG3.Overexpression of mi R-532-5p,silencing of PEG3 or pretreatment with sevoflurane can improve the motor function injury caused by spinal cord ischemia reperfusion injury,alleviate the apoptosis of spinal cord anterior horn motor neurons,reduce the permeability of BSCB,and inhibit the expression of PEG3.It also inhibited the release of inflammatory factors such as IL-1β,TNF-α,IL-6.TUNEL staining was used to detect cell apoptosis in each groupResults: The expression of mi R-532-5p in IR group was significantly decreased while the expression of PEG3 was significantly increased,compared with Sham group.PEG3 is the target protein of mi R-532-5p,and mi R-532-5p can inhibit the expression of PEG3.Overexpression of mi R-532-5p,PEG3 silence or sevoflurane pretreatment can improve the motor function injury caused by SCIRI,alleviate the apoptosis of motor neurons in the anterior horn of the spinal cord,reduce the permeability of BSCB,inhibit the expression of PEG3,and reduce the release of IL-1β,TNF-α and IL-6 inflammatory factors.Inhibition of mi R-532-5p can aggravate spinal cord injury.Sevoflurane pretreatment increased the expression of mi R-532-5p and decreased the expression of PEG3 protein in rats with SCIRI.Conclusions: SCIRI mi R-532-5p expression in lower,higher PEG3 protein expression.mi R-532-5p inhibits post-transcriptional expression by targeting PEG3 to alleviate neuroinflammation and apoptosis in SCIRI and protect neuronal function.Sevoflurane preconditioning has a protective effect on SCIRI through mi R-532-5p/PEG3.