Microglia-associated neuroinflammation is a potential therapeutic target for ischemic stroke

Microglia-associated neuroinflammation plays an important role in the pathophysiology of ischemic stroke.Microglial activation and polarization,and the inflammatory response mediated by these cells play important roles in the development,progression and outcome of brain injury after ischemic stroke.Currently,there is no effective strategy for treating ischemic stroke in clinical practice.Therefore,it is clinically important to study the role and regulation of microglia in stroke.In this review,we discuss the involvement of microglia in the neuroinflammatory process in ischemic stroke,with the aim of providing a better understanding of the relationship between ischemic stroke and microglia.

Study on the protective effect of Tadehaginoside on the damage of endothelial cell mitochondria induced by reactive nitrogen

Objective:To investigate the protective effect of Tadehaginoside on vascular endothelial cell injury induced by reactive nitrogen.Methods:MTT colorimetry was used to detect the effect of Tadehaginoside on the survival rate of EA.hy 926 endothelial cells in the concentration range of 5~160μmol/L;1 h after pre-administration of Tadehaginoside,0.5 mM GSNO was given to damage endothelial cells.Detect the mitochondrial specific factors COX-1,ND-1 and inflammatory factor IL-1βof EA.hy 926 cells damaged by GSNO by Real time-PCR method gene intervention.At the same time,Western blot was used to detect the changes in Bax and Bcl-2 protein expression.The mitochondrial membrane potential kit(JC-1)was used to detect the change of Tadehaginoside on the mitochondrial membrane potential after GSNO induced EA.hy 926 cell injury.Results:The results of the MTT method showed that Tadehaginoside had no obvious cytotoxicity on EA.hy 926 cells in the range of 5~160μmol/L,and the optimal protective concentration of the drug was 40μmol/L.Western Blot method showed that BAX protein expression increased in a time-dependent manner after GSNO damaged EA.hy 926 cells over time,while Bcl-2 protein expression was the opposite.Real time-PCR results showed that Tadehaginoside can significantly up-regulate COX-1 gene(P<0.05),and can significantly inhibit GSNO induced ND-1(P<0.05)and IL-1βgene up-regulation(P<0.01).At the same time,the results of JC-1 showed that Tadehaginoside could significantly protect the mitochondrial membrane potential from GSNO damage.Conclusion:The GSNO damage model may induce the increase of Bax and other pro-apoptotic proteins through mitochondrial DNA damage and reduce the expression of anti-apoptotic factor Bcl-2.Tadehaginoside has a certain protective effect on endothelial cell mitochondrial damage induced by reactive nitrogen,and its mechanism is related to inhibiting the expression of ND-1 and IL-1βgenes and upregulating the expression of COX-1 genes.