Expression Of Sox11 In Brain Tissue After Intracerebral Hemorrhage In Rat And Its Effect On Secondary Brain Injury

Background:Intracerebral hemorrhage(ICH)is a common acute central nervous system disease with rapid onset,high disability and lethality.Brain injury caused by ICH includes primary brain injury(PBI)and secondary brain injury(SBI).Sox11 is an important transcription factor of the Sox family.It is widely expressed in the developing nervous system and plays an important role in neurogenesis,neuron survival,and axonal growth.After cerebral ischemia in rats,the expression of Sox11 increased significantly.However,to date,the relationship between Sox11 and ICH is unclear.The main purpose of this study is to explore the spatiotemporal expression of Sox11 after ICH and its effect on secondary brain injury.Objective:1,To observe the expression of Sox11 in rat brain tissue and its change trend after intracerebral hemorrhage.2,To investigate the effects of Sox11 on secondary brain injury in rats after ICH and its possible mechanism.Methods:Part ? experiment:a sufficient number of rats were randomly selected from healthy adult male sprague-dawley(SD)rats.A total of 7 experimental groups were designed,namely Sham group,post-ICH 6h group,post-ICH 12h group,post-ICH 24h group,post-ICH 48h group,post-ICH 72h group,post-ICH 168h group,and the selected rats were randomly distributed among the 7 groups according to the cardinal number of 6 in each group.The ICH model was established by injecting heart autologous blood into the right basal ganglia of rats,and all rats were sacrificed at the corresponding time points set after ICH.After that,the samples of brain tissue were treated for Western blot experiments and immunofluorescence staining experiments.Through this part of the experiment,we can observe the expression of Sox11 and its changing trend after ICH,and perform corresponding statistical analysis.Part ? experiment:according to the results of the first part of the experiment,the 72h time point after ICH was selected as the standard point for this part of the experiment.First,a sufficient number of rats were randomly selected from healthy adult male SD rats.A total of 6 experimental groups were designed,namely Sham group,ICH group,ICH+vector group,ICH+over-Sox11 group,ICH+Si-control group,ICH+Si-Sox11 group.The selected rats were randomly distributed to these 6 groups accord ing to the base number of 12 in each group.Six rats were taken from each group,and the serum and cerebrospinal fluid of the rats were collected at 72h after ICH for ELISA to determine the level of TNF-? and IL-1?.Then the rats were sacrificed and the brain tissues was extracted as a sample specimen for Western blot,immunofluorescence staining experiment,TUNEL staining,FJC staining;an additional six rats in each group were used for the Morris water maze test,Rotarod performance test,neurological score evaluation and cerebral edema analysis.Results:Part ? experiment:the expression of Sox11 in the brain tissue increased after ICH,the increase was most obvious at 72h after ICH,and Sox11 was mainly expressed in neurons.Therefore,we chose the time point of 72h after ICH as the experimental standard point for subsequent experiments.Part ? experiment:at 72h after ICH,compared with the ICH+Si-Control group,the expression level of Sox11 in the ICH+Si-Sox11 group decreased significantly;compared with the ICH+Vector group,the expression level of Sox11 in the ICH+Over-Sox11 group increased significantly.Overexpression of Sox11 can reduce neuronal necrosis and apoptosis in rat brain tissue,reduce inflammatory response,cerebral edema,learning and cognitive dysfunction,vestibular motor dysfunction and neurological dysfunction caused by ICH.In contrast,after inhibiting the expression of Sox11,neuronal necrosis and apoptosis of rat brain tissue increased,inflammatory response and cerebral edema aggravated,learning and cognitive functions,vestibular motor function and neural function of rats were further impaired.Conclusions:the expression of Sox11 increased after intracerebral hemorrhage in rats,and the increase was most pronounced at 72h after ICH,Sox11 could play a neuroprotective role in secondary brain injury after ICH in rats.