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To Investigate Express And Changes Of Nervous Function On Cer-ebral Infarction Area, Apoptosis Regulatory Porteins, TNF-α、GFAP、BDNF Nestin And NSE After Cerebral Infarction In Rats

Posted on:2014-04-28Degree:MasterType:Thesis
Country:ChinaCandidate:J J CaoFull Text:PDF
GTID:2254330425958286Subject:Internal Medicine
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Objective:To investigate the relationship and significance of cerebral infarction oninfarction site histology and infarct area, nerve function and apoptosis proteins,inflammation and neurotrophic factor expression, neuronal and glial cell regenerationand so on at different times, to provide experimental basis for brain protective agent..Methods:1、Reperfusion model in rats was induced by the intraluminal suture method andrandomly divided into model1d group,3d group,7d group,14d group,21d group.2、The mNSS was performed at nerve function evaluation of MCAO rats.3、Histopathological changes and changes of the cerebral infarction area wereobserved by adopting HE staining method.4、Immunohistochemistry was used to detect the expressions of GFAP,NSE,BDNF, Nestin, TNF-a.Results:1、On the3rdday after MCAO, it’s been observed that cortical edema, fuzzyneuron structure but with clearly visible nuclei, basal ganglia region nerve fibersswelling and increasing astrocytes constituted the situation; Cortical neuron axonreduced or even extinguished, nucleolus became fuzzy, microglia appearedswallowing nerve,basal ganglia region nerve fibers disintegrated and microgliaincreased on the7thday; Neuron structure was not clear, basal ganglia region wascovered with microglia on the14thday; Fuzzy neuron structure, more basal gangliaregion microglia, newly-emerged fibrous connective tissue and blank area formed byischemic core area made up the recording situations on the21stday.2、Area of cerebral infarction gradually increased over time and infarctive regionexpanded from basal ganglia region to ischemic penumbra and finally reaching tocortical areas after MCAO. The area on the model21d group day was apparently larger than that on the model1group,the3d group and the model7d group. The areaon the model14d group was apparently larger than that on the model1d group to themodel7d group. The area on the model7d group was apparently larger than that onthe model1d group (P0.05).3、The mNSS score gradually decreased over time after MCAO, of which therecording on the model21d group was significantly less than that on the model1dgroup (P<0.05).4、Bax staining area was mainly distributed over the cytoplasm and cellmembrane in the area of cortex and infarctive region’s basal ganglia region. Thenucleus of positive cells changed from clear to fuzzy until disappearing over time.Bax’s integrated optical density (IOD) began to decrease and reached the minimumon the model21d group, which was significantly less than that on the model1d group,model3d group, the model7d group and the model14d group (P<0.05). Bcl-2positive cells mainly distributed over the cytoplasm and cell membrane in the area ofcortex and ischemic penumbra. Positive cells increased gradually over time. Theamount on the model1d group and the model3d group were significantly less thanthat on the model14d group and the model21d group. The model7d group wassignificantly less than the model21d group (P0.05).5、TNF-α expression gradually increased until reaching the peak from the1dgroup to the7d group after MCAO.6、 After MCAO, GFAP positive cells mainly crowded around the infarctionarea. The numbers of GFAP positive cells appear two-way response with the passageof time. It gradually increased at model1,3d and7d group, gradually decreased atmodel14d group and model21d group. model7d group was significant more thanthose at model1d group and model3d group (P0.05).7、BDNF+positive cells staining mainly located in the cytoplasm and cellmembrane after MCAO. BDNF’s integrated optical density (IOD) appear two-wayresponse, it began to decrease at model1d group3d group,7d group and14d group,increase at day model21d group. Model1d group and21d group was significant more than at model14d group (P0.05).8、The amount of Nestin positive cells presented a two-way response with thepassage of time. It rose from model1d to7d group,after model7d group itgradually decreased.Model7d group was significantly greater than that at model1dgroup and model3d group(P<0.05).9、NSE integrated optical density (IOD) increased gradually. Model1d groupwas significantly less than that at model3d group,7d group,14d group and21dgroup. Model21d group was significantly greater than those at model3d group andmodel7d group(P<0.05).Conclusion:After MCAO, before day14, at first inflammation aggravated and then leads toapoptosis and glial cell proliferation, the repair of neural stem cell proliferation anddifferentiation started. After day14although cerebral infarction area and the braindamage was still increasing, resistance to apoptosis significantly enhanced andneurotrophic factors increased result in partial ischemia/hypoxia of nerve cells(ischemia half dark area) be protected and recovery of cellular function, neural stemcells proliferation and differentiation cause nerve cell regeneration. So nerve functionimproved significantly after day14.
Keywords/Search Tags:rat, MCAO, Brain ischemia, Glial fibrillary acidic protein (GFAP), Neuron-Specific Enolase (NSE), HE staining, TNF-α, Bax, Bcl-2, apoptosis, BDNF, Nestin, modified neurological severity score (mNSS)
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