异氟烷预处理对大鼠脑缺血再灌注损伤的作用及机制  

EFFECT AND MECHANISM OF ISOFLURANE PRECONDITIONING ON CEREBRAL ISCHEMIA/REPERFUSION INJURY IN RATS

作　　者：朱婧 赵义康 王臻[1] 常建华 张世平[1] ZHU Jing;ZHAO Yikang;WANG Zhen;CHANG Jianhua;ZHANG Shiping(Department of Anaesthesiology,Shanxi Provincial People’s Hospital,Xi′an 710000,China)

机构地区：[1]陕西省人民医院麻醉科,陕西西安710000

出　　处：《青岛大学学报（医学版）》2021年第2期255-259,共5页Journal of Qingdao University(Medical Sciences)

基　　金：陕西省自然科学基础研究计划项目(2018JM7121)。

摘　　要：目的探讨异氟烷(ISO)预处理对脑缺血再灌注(I/R)损伤的影响及其机制。方法用线栓法构建I/R模型,将50只大鼠随机分为5组:假手术组(A组)、I/R组(B组)、I/R+ISO组(C组)、I/R+ISO+吡咯烷二硫代氨基甲酸铵(PDTC)组(D组)和I/R+ISO+二甲基亚砜(DMSO)组(E组),每组10只。用Longa评分法评估各组大鼠神经功能损伤评分和TMS评分,TTC法检测脑组织梗死面积,TUNEL法检测神经细胞凋亡率,ELISA法检测脑组织中肿瘤坏死因子α(TNF-α)和白细胞介素1β(IL-1β)的含量,Western blot检测脑组织中Bcl-2、Cleaved Caspase-3和NF-κB p65蛋白的表达。结果与A组相比较,B、C、D和E组的TMS评分、Bcl-2表达水平均明显降低,而神经功能损伤评分、神经细胞凋亡率和脑组织梗死面积、NF-κB p65和Cleaved Caspase-3表达水平、TNF-α和IL-1β含量均明显升高(P<0.05)。与B组相比,C、D和E组以上各指标有不同程度的逆转(P<0.05)。而C组和D组比较、C组与E组比较差异无显著性(P>0.05)。结论ISO预处理可保护脑I/R损伤,其作用机制可能与抑制NF-κB信号通路减少神经细胞凋亡和减轻炎症反应有关。Objective To investigate the effect and mechanism of isoflurane(ISO)preconditioning on cerebral ischemia/reperfusion(I/R)injury.Methods The suture method was used to establish an I/R model,and 50 rats were randomly divided into sham-operation group(group A),I/R group(group B),I/R+ISO group(group C),I/R+ISO+pyrrolidine dithiocarbamate(PDTC)group(group D),and I/R+ISO+dimethyl sulfoxide(DMSO)group(group E),with 10 rats in each group.The Longa scoring method was used to evaluate the neurological deficit score of each group;the TTC method was used to measure brain infarct area;the TUNEL method was used to measure the apoptosis rate of neural cells;the ELISA method was used to measure the content of tumor necrosis factor-α(TNF-α)and interleukin-1β(IL-1β)in brain tissue;Western blot was used to measure the protein expression of Bcl-2,cleaved caspase-3,and NF-κB p65 in brain tissue.Results Compared with group A,groups B,C,D,and E had significant reductions in TMS score and the expression level of Bcl-2 and significant increases in neurological deficit score,apoptosis rate of neural cells,brain infarct area,expression levels of NF-κB p65 and cleaved caspase-3,and levels of TNF-αand IL-1β(P<0.05).Compared with group B,groups C,D,and E had varying degrees of reversal of the above indices(P<0.05).There were no significant differences between group C and group D and between group C and group E(P>0.05).Conclusion ISO pretreatment can protect the brain against I/R injury,possibly by inhibiting the NF-κB signaling pathway to reduce neural cell apoptosis and alleviate inflammatory response.

关 键 词：再灌注损伤 脑梗死 异氟醚 细胞凋亡 炎症 NF-ΚB信号通路 大鼠 

分 类 号：R977.6[医药卫生—药品] R364.1[医药卫生—药学]