β-1,3-半乳糖基转移酶2对脑缺血损伤模型小鼠脑损伤的作用及其机制  

Effect and mechanism ofβ-1,3-galactosyltransferase 2 on brain injury in cerebral ischemic injury mice model

作　　者：马丰源 刁赫 古岳 卢连生 范莉婕 王鹏 MA Fengyuan;DIAO He;GU Yue;LU Liansheng;FAN Lijie;WANG Peng(Department of Prosthodontics,School of Stomatology of Jinzhou Medical University,Jinzhou 121000,China;Department of Radiology,The First Affiliated Hospital of Jinzhou Medical University,Jinzhou 121000,China;Department of Infectious Diseases,The First Affiliated Hospital of Jinzhou Medical University,Jinzhou 121000,China;Department of Neurobiology,College of Basic Medical Sciences,Jinzhou Medical University,Liaoning Provincial Key Laboratory of Neurodegenerative Diseases,Jinzhou 121000,China)

机构地区：[1]锦州医科大学口腔医学院口腔修复科,辽宁锦州121000 [2]锦州医科大学第一附属医院放射科,辽宁锦州121000 [3]锦州医科大学第一附属医院传染科,辽宁锦州121000 [4]锦州医科大学基础医学院神经生物学教研室,辽宁省神经退行性疾病重点实验室,辽宁锦州121000

出　　处：《中国医科大学学报》2024年第8期736-740,共5页Journal of China Medical University

基　　金：国家级大学生创新创业训练计划(202210160016);辽宁省自然科学基金(2022-MS-391)。

摘　　要：目的探讨β-1,3-半乳糖基转移酶2(B3galt2)对脑缺血损伤模型小鼠脑损伤的作用及其机制。方法将成年雄性C57BL/6J小鼠随机分为假手术组(Sham组)、大脑中动脉栓塞(middle cerebral artery occlusion,MCAO)模型组、MCAO模型+慢病毒载体对照组(LV-GFP组)、MCAO模型+慢病毒载体过表达B3galt2组(LV-B3galt2组),每组6只。各组小鼠于脑缺血24 h后进行神经功能缺损评分和旋转棒实验,采用2,3,5-三氨基苯甲四氮唑染色测定脑梗死体积,采用尼氏染色法观察各组小鼠脑缺血半影区神经元数量,检测各组小鼠脑组织中氧化应激相关因子水平。结果与Sham组比较,MCAO模型组小鼠脑梗死体积增大,神经功能缺损明显(P<0.05),脑缺血区神经元数量明显减少,活性氧(ROS)和丙二醛(MDA)水平明显升高(均P<0.05),超氧化物歧化酶(SOD)和谷胱甘肽(GSH)水平明显降低(均P<0.05);与MCAO模型组比较,LV-B3galt2组小鼠脑梗死体积减小,神经功能明显改善(P<0.05),脑缺血区神经元数量明显增加,ROS和MDA水平明显降低(均P<0.05),SOD和GSH水平明显升高(均P<0.05)。结论B3galt2过表达可以减轻脑缺血损伤模型小鼠脑损伤,其作用机制可能是通过抑制氧化应激反应实现的。Objective To explore the role ofβ-1,3-galactosyltransferase 2(B3galt2)in mice with cerebral ischemic injury.Methods Adult male C57BL/6J mice were randomly divided into the sham,suture-occluded middle cerebral artery occlusion(MCAO)model,MCAO model+lentiviral vector control(LV-GFP),and MCAO model+lentiviral vector overexpression B3galt2(LV-B3galt2)groups,with six mice in each group.Neurological deficit scoring and rotating rod experiments were performed 24 h after ischemia in each group,and 2,3,5-triphenyltetrazolium chloride(TTC)staining was used to determine the infarction volume.The number of neurons in the ischemic cerebral cortex was determined in each group using Nissl staining.The levels of oxidative stress-related factors in the brain tissues were detected using the relevant kits.Results Compared with the sham group,the MCAO model group showed increased infarct volume and neurological deficits(P<0.05),significantly decreased number of neurons in the ischemic cerebral cortex and levels of super-oxide dismutase(SOD)and glutathione peroxidase(GSH)(all P<0.05),and significantly increased levels of reactive oxygen species(ROS)and malondialdehyde(MDA)(all P<0.05).Compared with the MCAO model group,the LV-B3galt2 group had reduced volume of cerebral infarction,significantly improved neurological deficits(all P<0.05),significantly increased number of neurons in the ischemic cerebral cortex of mice,significantly decreased levels of ROS and MDA(P<0.05),and significantly elevated levels of SOD and GSH(all P<0.05).Conclusion B3galt2 overexpression can reduce brain injury in an ischemic damage mouse model,and its mechanism may be through the inhibition of oxidative stress reactions.

关 键 词：β-1 3-半乳糖基转移酶2 脑缺血损伤模型小鼠 脑损伤 

分 类 号：R743.3[医药卫生—神经病学与精神病学]