| Stroke is a serious threat to human health,divided into ischemic stroke and hemorrhagic stroke.Among them,acute ischemic stroke is a cerebral tissue infarction caused by cerebral arterial infarction,which is the most important death and disability of the central nervous system vascular events in modern society.It was found that Toll-like receptor 2(TLR2),matrix metalloproteinase 2(MMP-2)and matrix metalloproteinase 9(MMP-9)all played a role in the brain injury after acute ischemic stroke,involving the destruction of the blood-brain barrier.But it is not clear whether TLR2 has the function of regulating the brain’s microvascular endothelial cells MMP-2/9,and whether TLR2 causes blood-brain barrier damage by raising MMP-2/9 after acute cerebral ischemia.To this end,this paper intends to study the changes of cerebral microvascular endothelial cells TLR2 and MMP-2/9 by making a model of arterial embolism(MCAO)in the brains of rats,and to observe the changes of MMP-2/9 and blood-brain barriers by making tatters embolism re-injection(MCAO)models,and giving TLR2 agonisors and antagonists.The introduction of acute cerebral ischemic endothelial cells MMP-2/9 upward and its possible mechanism;the role of TLR2 in acute cerebral ischemic post-hematomy barrier injury;TLR2-specific ligand Pam3CSK4 and TLR2-specific antibody T2.5 in the treatment of acute cerebral ischemic post-brain barrier in the clinical significance.Objective: To explore the changes of TLR2 and MMP-2/9 of the endothelial cells of the cerebrovascular endothelial cells after acute cerebral ischemic re-injection in rats,and to give TLR2 agonist and antagonist treatment,to observe the changes of MMP-2/9,and to explore the possible treatment prospects of TLR2 antagonists in ischemic re-injection brain injury.Methods: Using thrombosis method to make arterial embolism re-perfusion(MCAO)model in the brains of rats,the change of cerebral ischemia volume was measured by TTC staining method,and the microvascular endothelial cells at different points of time were obtained by micro-laser cutting,and the expression of MRNA between TLR2 and MMP-2/9 by RT-PCR method.Results: After 1h,3h,6h and 24 h of brain ischemia in rats,the expression of m RNA in TLR2,MMP-2/9 increased over time.After being treated with TLR2-specific ligand Pam3CSK4,the expression of TLR2,MMP-2/9 increased over time,but the magnitude increase was higher than that of the untreated group,and at 24 h point-in-time,the Pam3CSK4 processing group had a statistical difference(p<0.05)compared to the increase in m RNA expression level of the unprocessed group of TLR2,MMP-2/9(p<0.05).After TLR2-specific antibody T2.5 treatment was given,the m RNA expression of TLR2,MMP-2/9 was still increased over time,but the amplitude of the increase was decreased compared to the untreated group,and at 6h time point,the T2.5 treatment group compared to the increase of MMP-9 expression level in the untreated group.There was a statistical difference(p<0.05),and at 24 h point-in-time,there was a statistical difference(p<0.05)compared to the increase in TLR2 and MMP-2 expression levels in the unprocessed group at 24 h point-in-timeConclusion: After 24 h,ischemic cerebrovascular endothelial cells TLR2 and MMP-2/9 were all raised,and were likely to be involved in ischemic brain injury.Ischemic re-perfusion is given to the TLR2 agonist Pam3CSK4,which can increase the m RNA increase of TLR2,MMP-2/9.The increase of m RNA of MMP-2/9 can be reduced after re-perfusion given TLR2-specific antibody T2.5,indicating that it may reduce the damage of the acute brain ischemic re-infusion of the microvascular endothelial cells of the brain. |
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