| ObjectivesTo observe the effect of GLP-1 receptor agonist exenatide on inflammatory reactions in rats with ischemia-reperfusion to explore the neuroprotective effect of exenatide in order to provide experimental basis for the treatment of ischemic stroke.MethodsHealthy male Wistar rats were randomly divided into control group,MCAO group and exenatide intervention group.Rats in the control group only underwent sham operation without blocking blood vessels and rats in the model group were made focal ischemiareperfusion model by MCAO method while rats in the exenatide intervention group were made by the same method as those in the model group,but they were intervened by intraperitoneal injection of exenatide immediately after reperfusion.The neurological function of rats in each group was evaluated after 1 hour of ischemia and 24 hours of reperfusion.After that,the rats were killed to get the brains immediately.TTC staining was used to determine the volume of cerebral infarction in rats of each group.Hippocampus was isolated,then the MPO activity was measured in each group.m RNA expression levels of inflammatory related factors IL-6,TNF-α and NF-κB in cortex and hippocampus of rats in each group were determined by fluorescence quantitative polymerase chain reaction method.Protein expression levels of p-P65 NF-κB,total P65 NF-κB,IL-6 and TNF-α in cortex and hippocampus of rats of each group were determined by Western blotting.Results1.There were no neurological deficit symptoms in the control group,and the neurological deficit symptoms in the model group and the exenatide intervention group were obvious,but compared with the model group,the neurological function score of the exenatide intervention group was significantly lower.2.After TTC staining,the control group had no infarct focus,and the model group and the exenatide intervention group had obvious infarct focus,but compared with the model group,the infarct volume of the exenatide intervention group was lower.3.The MPO activity in the hippocampus of rats in the control group was very low,while the MPO activity in the hippocampus of rats in the model group and the exenatide intervention group was significantly increased,but compared with the model group,the MPO activity in the hippocampus of rats in the exenatide intervention group was significantly decreased.4.The m RNA expression levels of IL-6,TNF-α and NF-κB in the control group were lower,but the expression levels of the three factors in the model group and the intervention group were significantly higher.The expression levels of these three factors in the exenatide intervention group were significantly lower than those in the model group,and the results of hippocampus and cortex were consistent.5.The expression levels of p-P65 NF-κB protein and total P65 NF-κB protein,IL-6protein and TNF-αprotein were significantly higher than those of the control group.But the expressions of p-P65 NF-κB protein,IL-6 protein and TNF-α protein in the exenatide intervention group were significantly lower than those in the model group.The results of hippocampus and cortex were consistent.Conclusions1.Exenatide intervention can reduce cerebral infarction volume,relieve neurological deficit symptoms and play a neuroprotective role in MCAO rats.2.Exenatide may play a neuroprotective role by inhibiting the occurrence of inflammatory reaction. |
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