异氟烷对脑缺血再灌注损伤大鼠神经细胞损伤的影响及机制研究  

EFFECTS AND MECHANISM OF ISOFLURANE ON NEURONS DAMAGE IN RATS WITH CEREBRAL ISCHEMIA-REPERFUSION INJURY

作　　者：张燕 刘勇[2] 戚扬颂 ZHANG Yan;LIU Yong;QI Yangsong(Department of Anesthesiolo-fry t Hainan Modern Women and Childrens Hospital,Haikou 570000,China)

机构地区：[1]海南现代妇女儿童医院麻醉科,海南省海口市570000 [2]新疆医科大学第四附属医院麻醉科

出　　处：《中国煤炭工业医学杂志》2021年第3期236-241,共6页Chinese Journal of Coal Industry Medicine

基　　金：新疆维吾尔自治区科学技术厅项目(编号:2016D01C52)。

摘　　要：目的探讨异氟烷对局灶性脑缺血再灌注(FCIR)损伤大鼠神经细胞线粒体损伤及c-Jun氨基末端激酶(JNK)表达的影响。方法将72只SD大鼠分为空白组、假手术组、FCIR组、异氟烷组,FCIR组、异氟烷组运用线栓法制备FCIR损伤大鼠模型,异氟烷组再灌注时吸入1.5%异氟烷1 h,观察各组FCIR损伤大鼠再灌注24 h后神经损伤、脑梗死体积、脑组织凋亡、神经细胞线粒体损伤情况。结果与假手术组比较,FCIR组、异氟烷组的神经功能评分、脑梗死体积和神经细胞线粒体膜电位绿色荧光强度、线粒体基质Ca2+浓度显著升高(P<0.05),脑组织凋亡率、Caspase-3、Bax、Cyt C、p-JNK/JNK蛋白水平升高(P<0.05),ATP含量、Na^(+-)K^(+-)ATPase活性、Bcl-2蛋白水平降低(P<0.05);与FCIR组比较,异氟烷组神经功能评分、脑梗死体积和神经线粒体膜电位绿色荧光强度、线粒体基质Ca2+浓度降低(P<0.05),脑组织凋亡率、Caspase-3、Bax、Cyt C、p-JNK/JNK蛋白水平降低(P<0.05),ATP含量、Na^(+-)K^(+-)ATPase活性、Bcl-2蛋白水平升高(P<0.05)。结论异氟烷可降低FCIR损伤大鼠神经元凋亡、改善神经细胞的线粒体损伤,可能与降低pJNK/JNK蛋白水平有关。Objective To explore the effects of isoflurane on mitochondrial injury of neurons and expression of c-Jun N-terminal kinase(JNK) in rats with focal cerebral ischemia-reperfusion(FCIR) injury.Methods Seventy-two SD rats were divided into blank group, sham operation group, FCIR group and isoflurane group.In FCIR group and isoflurane group, FCIR injury rat models were prepared by suture method.The isoflurane group was given 1.5% isoflurane inhalation for 1 h during reperfusion.The nerve injury, cerebral infarction volume, apoptosis of brain tissue and mitochondrial injury of neurons after 24 h of reperfusion in FCIR injury rats in each group were observed.Results Compared with sham operation group, nerve function score, cerebral infarction volume, green fluorescence intensity of neuronal mitochondrial membrane potential, and concentration of mitochondrial matrix Ca2+ were significantly increased in FCIR group and isoflurane group(P<0.05),apoptosis rate of brain tissue, levels of Caspase-3,Bax, Cyt C and p-JNK/JNK proteins were increased(P<0.05),ATP content, activity of Na^(+-)K^(+-)ATPase and level of Bcl-2 protein were decreased(P<0.05).Compared with FCIR group, nerve function score, cerebral infarction volume, green fluorescence intensity of neuronal mitochondrial membrane potential, and concentration of mitochondrial matrix Ca2+ were decreased in isoflurane group(P<0.05),apoptosis rate of brain tissue, levels of Caspase-3,Bax, Cyt C and p-JNK/JNK proteins were decreased(P<0.05),ATP content, activity of Na^(+-)K^(+-)ATPase and level of Bcl-2 protein were increased(P<0.05).Conclusion Isoflurane can reduce neuronal apoptosis and improve mitochondrial injury of neurons in rats with FCIR injury, which may be related to decreasing level of p-JNK/JNK protein.

关 键 词：局灶性脑缺血再灌注损伤 异氟烷 线粒体损伤 神经元凋亡 C-JUN氨基末端激酶 

分 类 号：R614[医药卫生—麻醉学]