| Objective:Ischemic stroke brings great harm to human health and social economy.As China's population age structure gradually develops toward an aging trend,reducing the burden caused by ischemic stroke is an urgent task.In this study,theischemia/reperfusionmodel and ischemic postconditioning model were established after the MCAO model by the suture-occluded method in the rat.The differential expression of lncRNAs in theischemic postconditioning model group were screened out,and the expression of LC3-? and Beclinl in the brain tissue were detected.So as to study the role of ischemic postconditioning in regulating IncRNAs in the process of autophagy.Methods:(1)The ischemia/reperfusionmodel and ischemic postconditioning model were established after the MCAO model by the suture-occluded method.The modified mNSS neurological function score were used to assess neurological function after intervention and TTC staining to measure the infarct volume.(2)The lncRNAs chip was used to screen out the differential expression of IncRNAs in theischemic postconditioning model group.(3)The expression of LC3-? and Beclinl protein were detected by Western Blot and Q-PCR was used to detect the expression of LC3-? and Beclinl.In order to study the autophagy regulated by LC3-? and Beclinl involves in the protective effects of ischemic postconditioning on cerebral ischemia-reperfusion injury in rats.Results:(1)MCAO model in the male SD rats were successful established:hemiparalysis on contralateral limbs of occlusionoccurred in the enrolled rats,manifested as the performance of neurological deficits such as inability to walk straightly and flexion of the contralateral limbswhen the tail was lifted.7-12 points of Neurological deficit mNSS score was the eligible requirement.After TTC staining,it was confirmed that the blood supply area of middle cerebral artery in the right brain of the rat was white and the normal brain tissue was red.Compared with I/R group,rats in IPostC group had lower scores of neurological deficits and improved symptoms after infarction(P<0.05,the difference was statistically significant);I/R group had larger infarct volume than IPostC group(P<0.05,the difference was statistically significant).(2)The expression profiles of IncRNAs in ischemic brains of IPostC group and I/R group were successfully screened.A total of 899 target IncRNAs were screened up or down-regulated by ? 2.0 and P-value? 0.05.There were 174 IncRNAs up-regulated in the IPostC group and 725 down-regulated lncRNAs.(3)Western Blot results showed that the protein expression of LC3-? and Beclinlin the ischemic postconditioning group was lower than that in the ischemia/reperfusion group,and the difference was statistically significant(P<0.05).Results of Q-PCR showed that the expression of LC3-? mRNA and Beclinl mRNA in the ischemic postconditioning group was lower than that in the ischemia/reperfusion group,and the difference was statistically significant(P<0.05).Conclusions:(1)Ischemic postconditioning has a protective effect on focal cerebral ischemia in rats.When blood is reperfused,it can effectively reduce reperfusion injury,reduce infarct volume and improve neurological deficits.(2)After ischemic postconditioning in rats with focal cerebral ischemia,the expression profiles of IncRNAs in brain alter significantly compared with direct blood flow reperfusion,and IncRNAs play an important role in the regulation of ischemic postconditioning.(3)Ischemic postconditioning provides brain protection effects in cerebral ischemia/reperfusion injury by inhibiting autophagy(down-regulating the expression of LC3-? and Beclin1).(4)Ischemic postconditioning may regulate autophagy by IncRNAs in cerebral ischemia/reperfusion injury. |
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