| Objective To study the activation of microglia and the expression of TLR4 receptor on microglia in the hippocampus of DEACMP animal model,and to clarify the mechanism of DEACMP from the mechanism of immune inflammation.Methods1.The cognitive qualified mice were randomly divided into the experimental group and the control group.The experimental group established the model of 40 min poisoning according to the static inhalation of carbon monoxide(CO)concentration of 3000 ppm and continuous inhalation of DEACMP,and the control group was filled with the same amount of air.2.On the 21 st day after poisoning,Morris water maze test and HE staining were used to observe the damage of hippocampal tissue and cells in order to determine the construction of DEACMP mouse model.3.The brain specimens of the two groups were taken and double-labeled immunofluorescence staining was performed to observe the co-expression of microglia specific markers Iba1 and TLR4 receptor.Result The results of water maze: there was significant difference in the navigation time between the experimental group and the control group before and after the experiment(P < 0.05),and there was significant difference between the experimental group and the control group after the experiment(P < 0.05).HE staining results: the results of HE staining of hippocampal tissue of experimental mice showed that the number of hippocampal tissue cells decreased,the cell structure was disordered,the nucleus was dissolved and the structure was unclear,but the hippocampal tissue cells of the control group were neatly arranged and the structurewas intact.In summary,the DEACMP mouse model was successfully established.2.The results of immunofluorescence staining showed that the co-expression of Iba1 and TLR4 in the hippocampus of the experimental group was significantly higher than that of the control group.Conclusion In microglia,TLR4 receptor may be involved in the pathogenesis of DEACMP. |
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