Mechanism of γδT cell receptor in global cerebral ischemia-reperfusion injury after cardiopulmonary-cerebral resuscitation in mice
To explore the mechanism of γδT cell receptor in global cerebral ischemia-reperfusion injury after cardiopulmonary-cerebral resuscitation(CPCR)in mice,adult male C57BL/6 mice were randomly divided into three groups: blank group,CPCR group,and CPCR + γδT receptor antagonist group.The model of global cerebral ischemia-reperfusion injury in mice after CPCR was established by asphyxia and then paraffin sections of mouse brain tissue were made.H-E staining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling(TUNEL)were used to observe the injury and apoptosis of cerebral tissue.Western blotting and immunohistochemistry were used to evaluate the protein expression levels of IL-17A and IL-23p19.The mRNA expression levels of IL-17A and IL-23p19 were evaluated by RT-PCR.The results showed that compared to those of the blank group,large numbers of cells in the central area of cerebral ischemia foci in the CPCR group were dead or showed irregular state of enlargement,rupture of nuclear membrane,and disappearance of cell structure.And the apoptosis in the CPCR group was more severe than that in blank group.In contrast,all the above manifestations were less severe in CPCR+ γδT receptor antagonist group.Compared to those in the blank group,the brain injury score,apoptosis rate,IL-17A and IL-23p19 expressions were significantly increased in the CPCR group(P＜0.01).Compared to the CPCR group,the CPCR+ γδT receptor antagonist group had significantly lower brain injury score,apoptosis rate,IL-17A and IL-23p19 expressions(P＜0.05).These results suggest that the γδT cell receptor plays a proinflammatory role in the pathogenesis of global cerebral ischemia-reperfusion injury after CPCR in mice by regulating the levels of IL-17A and IL-23p19 in γδT cells.
万方数据
维普
