The postoperative cognitive dysfunction induced by central inflammation with possible involvement of the gut-brain axis

被引:0
|
作者
Lin, Chuantao [1 ]
Wang, Jing [1 ]
Wang, Yuping [1 ]
Chen, Chanjuan [1 ]
Gao, Xiang [1 ]
机构
[1] Fujian Med Univ, Fujian Matern & Child Hlth Hosp, Coll Clin Med Obstet & Gynecol & Pediat, Dept Anesthesiol, Fuzhou, Fujian, Peoples R China
关键词
Postoperative cognitive dysfunction; Tibial fracture; CCL11; Gut -brain axis; PRESEPSIN SCD14-ST; DIAGNOSTIC-ACCURACY; SEPSIS; PROCALCITONIN; MACROPHAGES;
D O I
10.1016/j.clinsp.2022.100104
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Postoperative cognitive dysfunction is widely recognized as severe postoperative central nervous dys-function and has a significant impact on the 'patient's physical and mental health.Methods: Postoperative models of tibial fracture in aged rats were established, including the control group, model group, CCL11 protein injection group, and saline injection group. Morris water maze test was used to detect the behavioral characteristics of rats. Enzyme-Linked Immunosorbent Assay was used or determine the content of CCL11 and CXCL10. Immunofluorescence staining was used to detect the distribution of CD14+CD163+macro-phages in colon tissues and CD11b+CCR3+microglia cells in hippocampal tissues. Western blot analyzed NOX1 and STAT3 expression in hippocampus tissues.Results: Water maze test results confirmed severe cognitive impairment in CCL11 rats. The content of CCL11 and CXCL10 in the CCL11 group was much higher than that of the model group. The distribution of macrophage and microglia cells in the CCL11 model group was greater than that in the model group and the saline group. The expression of NOX1 and STAT3 in the CCL11 group was higher compared with the model group.Conclusion: Abnormal macrophage function and excessive CCL11 secretion were observed in the rats with lower limb fractures after surgery. Postoperative central inflammation in rats with lower limb fracture induced postop-erative cognitive dysfunction through the gut-brain axis molecular mechanism.
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页数:7
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