Effect of P2Y1 receptor activation on astrocytes in delayed encephalopathy after acute carbon monoxide poisoning / 中风与神经疾病杂志

ABSTRACT

@#Objective To investigate the role of P2Y1 receptors and astrocytes in delayed encephalopathy after acute CO poisoning (DEACMP) and the possible pathogenesis of DEACMP.Methods Male SD rats with acceptable cognitive function were screened by water maze test and randomly divided into two groups:the control group and the CO poisoning group.The poisoning group was subjected to DEACMP model.The behavioral changes,neuronal changes and the expressions of P2Y1 receptor and astrocytes in hippocampus of the two groups were compared at 7,14,21 and 28 d after modeling,respectively.Results Compared with the control group,the escape latencies of rats in the poisoning group were significantly prolonged on the 21st and 28th days after modeling (P<0.05).HE staining showed that the hippocampal pyramidal cells and neurons in the model group exhibited obvious necrosis on days 14,21,and 28 after modeling.The water maze indicated that DEACMP occurred on day 21.Compared with the control group,Western blot analysis showed that the expression levels of P2Y1 and GFAP proteins in the hippocampus of the poisoning group were increased at each time point (P<0.05),which increased first and then decreased.Immunofluorescence showed co-expression of P2Y1 and GFAP in hippocampus.Compared with the control group,the expressions of P2Y1 and GFAP in hippocampal CA1 region were up-regulated at each time point after poisoning (P<0.05). Conclusion The activation of astrocytes by P2Y1 receptor may be one of the pathogenesis of DEACMP,and astrocytes may impair learning and memory ability of co-poisoned rats by mediating immune inflammation,leading to DEACMP.