Effects Of Melatonin On Autophagy After Acute Spinal Cord Injury

Background and objectiveAs the most serious complications of spinal injury,acute spinal cord injury(acute spinal cord injury,ASCI)often cause physical sensory and dysfunction of serious damage.For the patient himself,it brings serious physical and psychological harm,which,for society as a whole,creates a huge financial burden.In view of this,today's medical community on acute spinal cord injury prevention,treatment and rehabilitation to give more and more attention and attention.With the development of pathophysiology,the understanding of acute spinal cord injury has gradually deepened,divided into primary and secondary spinal cord injury.As the current clinical can not interfere with primary spinal cord injury,secondary spinal cord injury plays an important role in ASCI,and neuronal apoptosis and secondary spinal cord injury is closely related to the occurrence.Therefore,inhibition of neuronal cell apoptosis has become the key to ASCI early treatment.Cell autophagy is a highly conserved biological self-protection mechanism that allows degenerative proteins and loss of functional organelles to be degraded and reused.In recent years,studies have confirmed that cell autophagy and apoptosis have a mutual influence.Melatonin(MT)is produced by the pineal gland and secretion of amphiphilic molecules,widely present in the body,the current scholars generally believe that melatonin by reducing edema,inhibition of apoptosis,reduce oxidative stress and other mechanisms to play its protective nerve The role.However,there is no consensus on the mechanism of melatonin in the treatment of spinal cord injury in anti-apoptotic mechanisms.Therefore,in this study,we investigated the effects of melatonin on autophagy by observing the occurrence of autophagy after acute spinal cord injury by observing melatonin in the ASCI animal model and studying the mechanism of melatonin Application provides reference.Material and Methods108 adult SD rats were randomly divided into three groups: sham operation group(group A),spinal cord injury group(group B)and melatonin treatment group(group C).A group of laminectomy only,exposed T11-T12 segment,does not damage the spinal cord nerve.The T11-T12 spinal cord injury model was established by modified Allen's method in group B and group C,and an equal volume of absolute ethanol and 100 mg / kg MT preparation were injected intraperitoneally 10 min after spinal cord injury.Twelve rats were randomly selected at 6 h,12 h and 24 h after operation.The expression levels of autophagy-related proteins were detected in 6 samples of T11-T12 segment spinal cord,6 HE staining and immunofluorescence Sliced to observe the spinal cord injury and repair.Basso Beattie Bresnahan(BBB)motor function scores were scored at 72 h postoperatively.ResultsAfter spinal cord injury,B and C groups had severe lower limb neurological dysfunction.At 72 hours after operation,the BBB motor function score of group C was significantly higher than that of group B(p <0.05).At the time of operation,(P <0.05).The expression level of light chain 3(LC3)in the microtubule-associated protein 1 was the highest in group C,the lowest in group B and the lowest in group A.(P <0.05).The expression level of Beclin-1 in the spinal cord of the rats at each time point was higher than that of the control group at the time of 6h,12 h and 24 h The lowest in group A.(P <0.05).HE staining was used to observe the degree of spinal cord injury: the lightest group in group A was the second,and the second group was the most important in group B,and the difference was statistically significant(P <0.05)at 6 h,12 h and 24 h,The longer the injury time of each group,the more severe the degree of injury;immunofluorescence showed: C group LC3 positive neuronal cells up to B group followed,A group at least.ConclusionAbdominal autogenesis occurs after early acute spinal cord injury in rats.The use of melatonin enhances autophagy and,to a certain extent,plays a role in protecting neurological function...