十溴二苯乙烷和豌豆肽对实验大鼠认知功能的影响  

Effects of DBDPE and pea peptide on cognitive function in experimental rat

作　　者：雷昌亭 郑刘根 杨永浩 赵祥忠 赵秀兰[1] 寇蕊蕊[1] Lei Changting;Zheng Liugen;Yang Yonghao;Zhao Xiangzhong;Zhao Xiulan;Kou Ruirui(School of Public Health,Shandong University,Jinan 250012,China;School of Food Science and Engineering,Qilu University of Technology,Jinan 250306,China)

机构地区：[1]山东大学公共卫生学院,山东济南250012 [2]齐鲁工业大学食品科学与工程学院,山东济南250306

出　　处：《兰州大学学报（医学版）》2023年第11期18-25,共8页Journal of Lanzhou University（Medical Sciences）

基　　金：山东省重点研发计划(重大科技创新工程)资助项目(2020CXGC10604)。

摘　　要：目的探讨十溴二苯乙烷对大鼠认知功能损伤及豌豆肽的干预作用。方法SPF级Wistar成年雄性大鼠40只,随机分为对照组、十溴二苯乙烷低剂量组、十溴二苯乙烷高剂量组、豌豆肽+十溴二苯乙烷高剂量组。十溴二苯乙烷经口染毒连续8周,同时经饮水给予豌豆肽干预,采用Morris水迷宫评价其空间学习记忆能力;制备大脑冰冻切片,分别采用免疫组织化学、尼氏染色、免疫荧光染色观察大脑胶质细胞的激活情况以及神经元的退行性变化及凋亡情况;采用Western blotting检测大脑皮层神经元突触蛋白synapsin-1和突触后密度蛋白95的蛋白表达水平。结果与对照组相比,十溴二苯乙烷低、高剂量组逃避潜伏期和游泳总路程明显增加,穿越平台次数显著降低(P<0.05);大脑神经元尼氏体染色变浅,细胞出现空泡样改变;免疫组织化学染色显示星形胶质细胞和小胶质细胞活化;免疫荧光染色显示大脑神经元发生凋亡,伴随突触蛋白synapsin-1和突触后密度蛋白95蛋白表达水平降低,且呈剂量依赖性变化(P<0.05)。大鼠染毒同时经饮水给予豌豆肽干预,神经行为学和大脑病理损伤均得到一定程度的改善(P<0.05)。结论十溴二苯乙烷暴露可导致大鼠大脑神经元和神经突触损伤、星形胶质细胞和小胶质细胞活化、神经元发生凋亡;豌豆肽能显著改善十溴二苯乙烷诱导的大鼠认知功能损伤。Objective To investigate the cognitive impairments in rats induced by decabromodiphenyl ethane(DBDPE)and the intervention effect of pea peptide.Methods Forty male SPF Wistar adult rats were randomly divided into a control group,decabromodiphenylethane low-dose group,decabromodiphenylethane high-dose group,and pea peptide+decabromodiphenylethane high-dose group.DBDPE and pea peptide were administered by gavage and drinking respectively for 8 consecutive weeks,and Morris water maze was used to evaluate their spatial learning and memory abilities.Frozen brain sections were prepared for immunohistochemical staining,Nissl staining and immunofluorescent double staining to observe the activation of glial cells,neuronal degenerative changes and apoptosis.Western blotting was used to detect the protein expression levels of synaptic proteins synapsin-1 and PSD95 in the brain.Results Compared with the control group,the DBDPE-exposed group showed significantly increased escape latency and total swimming distance,and significantly decreased platform crossings(P<0.05).Nissl staining of brain neurons showed lighter staining and vacuolar changes.Immunohistochemical staining showed activated astrocytes and microglia.Immunofluorescent double staining showed neuronal apoptosis in the brain,accompanied by decreased expression levels of synaptic proteins synapsin-1 and PSD95,which exhibited a dose-dependent change(P<0.05).Rats exposed to DBDPE and simultaneously treated with pea peptide in drinking water showed an improvement in the above neurobehavioral changes and brain pathological damage to some extent(P<0.05).Conclusions DBDPE exposure could lead to neuronal and synaptic damage in the rat brain,activation of astrocytes and microglia,and neuronal apoptosis.Pea peptide could significantly improve cognitive impairments induced by DBDPE in rats.

关 键 词：十溴二苯乙烷 豌豆肽 认知功能 突触蛋白 细胞凋亡 胶质细胞 

分 类 号：R994.6[医药卫生—毒理学]