| Background:Stroke is a cerebrovascular disease with a complicated pathogenesis.According to the pathogenesis,it can be divided into hemorrhagic stroke and ischemic stroke,of which about two-thirds are ischemic stroke.In my country,the mortality rate of ischemic stroke is increasing year by year,ranking first among urban and rural residents.At present,there is a certain time window for the clinical treatment of ischemic stroke,so the search for potential treatment methods has become an urgent problem to be solved.Omentin is a new type of adipokines.In recent years,clinical studies have found that the concentration of Omentin in human plasma is negatively correlated with the severity of ischemic brain injury and prognostic evaluation.However the systematic research of Omentin’s neuroprotective effect after ischemic brain injury in mice,and how it exerts neuroprotective effects are rarely reported.Purpose:This experiment is to initially explore whether Omentin has a protective effect on the nerves in the acute phase of cerebral ischemic injury in mice.Method:1.A focal cerebral ischemia(ischemic,ISC)model was established by photochemical damage method,and 2,3,5-Triphenyltetrazolium chloride(TTC)staining was used to evaluate the infarct volume after cerebral ischemic injury in mice.2.Immunofluorescence staining and Western blot were used to evaluate the transfection efficiency of Omentin recombinant adeno-associated virus and the cell types transfected.3.Fatigue rotary rod test,HE staining,TUNEL staining,immunofluorescence staining and Western blotting were used to evaluate the changes in indexes related to nerve function after injury.Results:1.Compared with the Sham group,the ischemic group(Isc group)formed a clear infarct area in the cerebral cortex.2.Compared with the Sham group,Omentin-positive cells were observed in the cortex of the Omentin AAV group(AAV-omentin group),and there was a high expression in the cortex at the injection point.About 43.5% of the Omentin-positive cells were compared with Neu N co-labeled,Omentin positive cells co-labeled with GFAP and Iba-1 were about 17.9% and4.8%.3.Compared with the Isc group and the Isc+AAV-con group,the mice in the Isc+AAV-omentin group did not lose weight,but the infarct volume was significantly reduced,and the time spent on the rotating rod increased;the damage area Neu N The amount and protein expression level increased significantly,and did not affect GFAP and Iba-1;it also reduced cell apoptosis and neuronal apoptosis;the expression of ZO-1,Occludin and Claudin-5 in the cortex of the injured area was also significantly up-regulated,and the blood vessel The density increased;at the same time,the number of M1 type microglia in the injured area was also significantly reduced.Conclusion:1.The model of focal cerebral ischemia was successfully established,and Omentin recombinant adeno-associated virus was highly expressed in the cortex at the injection point.2.Omentin can partially improve the motor function of mice in the acute phase of cerebral ischemic injury,and play a neuroprotective effect by reducing neuronal apoptosis,reducing the permeability of the blood-brain barrier and reducing the polarization of microglia to M1 type. |