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外周血炎性因子变化与术后认知功能障碍的关系 被引量:27

Relationship between postoperative cognitive dysfunction and the expression of inflammatory cytokines of plasma
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摘要 目的研究术后认知功能障碍(POCD)与外周血炎性因子之间的关系。方法选择于全身麻醉下行中大型骨科手术的患者40例,在术前1d及术后7d采用成套神经心理测验(BCAI)评价患者的认知功能。根据术后是否发生POCD分为POCD组(17例)及非POCD组(23例)。在认知功能测试的相应时间点分别采血,检测白细胞介素(IL)-1β、IL-1ra、IL-6、IL-8及肿瘤坏死因子(TNF)-α、TNF受体Ⅱ(TNFRⅡ)水平。结果两组手术前后均未检测出有IL-1β和TNF-α表达。与术前比较,POCD组术后促炎因子IL-6、IL-8表达均显著升高(P值均<0.05),抑炎因子IL-1ra、TNFRⅡ表达均显著降低(P值均<0.05)。非POCD组手术前后促炎因子和抑炎因子表达的差异均无统计学意义(P值均>0.05)。结论 POCD的发生与血浆中促炎因子IL-6、IL-8表达增加及抑炎因子IL-1ra、TNFRⅡ表达减少有关。 Objective To investigate the relationship between the expression of inflammatory factors in plasma and postoperative cognitive dysfunction(POCD). Methods The cognitive function of 40 patients undergoing operation under general anesthesia was evaluated by a battery of cognitive assessment instruments(BCAI) 1 d preoperatively and 7 d postoperatively.According to cognitive level,the patients were divided into cognitive dysfunction group(n=17) and non-cognitive dysfunction group(n=23).The levels of interleukin(IL)-1β,IL-1ra,IL-6,IL-8,tumor necrosis factor α(TNF-α) and tumor necrosis factor receptor Ⅱ(TNFRⅡ) were detected at the time set in advance. Results IL-1β and TNF-α were not detected in two groups preoperatively and postoperatively.Compared with the preoperative levels in cognitive dysfunction group,postoperative IL-6 and IL-8 were significantly increased(P0.05),and IL-1ra and TNFRⅡ were significantly decreased(P0.05).But the differences in expression of proinflammatory cytokines and anti-inflammatory cytokines in non-cognitive dysfunction group had no statistical significance before and after operation(P0.05). Conclusion POCD is associated with high expression of IL-6 and IL-8 and the low expression of IL-1ra and TNFRⅡ.
出处 《上海医学》 CAS CSCD 北大核心 2012年第2期115-117,共3页 Shanghai Medical Journal
基金 浦东新区科技发展基金创新基金(PKJ2008-Y27) 浦东新区卫生系统优秀青年医学人才培养计划(PWRq-2010-01)资助项目
关键词 术后认知功能障碍 炎症 白细胞介素-1拮抗剂 肿瘤坏死因子受体Ⅱ Postoperative cognitive dysfunction Inflammation Interleukin-1 receptor antagonist Tumor necrosis factor receptor Ⅱ
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