右美托咪定调控NLRP3炎症小体活化改善动物模型术后认知功能障碍的作用  

The effects of DEX in regulating NACHT,LRR and PYD domains-containing protein 3 inflammasome activation to improve postoperative cognitive dysfunction in rats

作　　者：项金慧 汪静 李兴[1] 仲勇[1] XIANG Jinhui;WANG Jing;LI Xing(Department of Anesthesiology,Shuguang Hospital Affiliated to Shanghai TCM University,Shanghai 201203,China)

机构地区：[1]上海中医药大学附属曙光医院麻醉科,上海市201203

出　　处：《河北医药》2022年第13期1934-1938,共5页Hebei Medical Journal

基　　金：国家自然科学基金(编号:81973652)。

摘　　要：目的 探讨右美托咪定(DEX)调控包含NACHT、LRR和PYD域的蛋白3(NLRP3)炎症小体活化改善术后认知功能障碍(POCD)的作用。方法 60只SD大鼠随机分为对照组、POCD组和POCD+DEX组,每组20例。通过吸入异氟醚建立大鼠POCD模型。术前30 min接受腹膜内注射DEX(20μg/kg)。检测3组大鼠的学习、记忆功能、海马神经元损伤和凋亡、NLRP3表达及NLRP3炎症小体活化蛋白白介素-1β(IL-1β)和半胱天冬酶-1(Caspase-1)的表达水平。结果 POCD组目标象限停留时间和穿越平台次数显著低于对照组,海马神经元损伤程度、凋亡指数、NLRP3、IL-1β和Caspase-1蛋白表达水平显著高于对照组(P<0.05)。POCD+DEX组的目标象限停留时间和穿越平台次数显著高于POCD组(P<0.05),海马神经元损伤程度、凋亡指数、NLRP3、IL-1β和Caspase-1蛋白表达水平显著低于POCD组(P<0.05)。结论 DEX能够保护POCD大鼠学习、记忆能力,并抑制NLRP3炎症小体激活抑制海马神经元凋亡。Objective To investigate the effects of dexmedetomidine(DEX)in regulating NACHT,LRR and PYD domains-containing protein 3(NLRP3)inflammasome activation to improve postoperative cognitive dysfunction(POCD)in rats.Methods Sixty SD rats were randomly divided into control group,POCD group and POCD+DEX group,with 20 rats in each group.The rat models with POCD were established by inhaling isoflurane,and DEX was injected intraperitoneally(20μg/kg)at 30min before surgery.The learning ability,memory function,hippocampal neuron damage and apoptosis,and the expression levels of NLRP3,NLRP3 inflammasome activation protein interleukin(IL)-1βand cysteinyl aspartate specific proteinase-1(Caspase-1)were observed and compared among the three groups.Results The target quadrant residence time and the number of crossing platforms in POCD group were significantly lower than those in control group,however,the damage degree of hippocampal neuron,apoptosis index,and the expression levels of NLRP3,IL-1βand Caspase-1 protein were significantly higher than those in control group(P<0.05).The target quadrant residence time and the number of crossing platforms in POCD+DEX group were significantly higher than those in POCD group(P<0.05),but,the damage degree of hippocampal neuron and apoptosis index,and the expression levels of NLRP3,IL-1βand Caspase-1 protein were significantly lower than those in POCD group(P<0.05).Conclusion DEX can protect the learning and memory abilities of rats with POCD,and inhibit the activation of NLRP3 inflammasomes to inhibit hippocampal neuronal apoptosis.

关 键 词：术后认知功能障碍 右美托咪定 PYD域的蛋白3炎症小体 凋亡 

分 类 号：R971.2[医药卫生—药品]