竹荪多糖对亚砷酸钠致大鼠神经毒性的保护作用  

Protective effect of Dictyophora polysaccharide on neurotoxicity induced by sodium arsenite in rats

作　　者：张兴来 胡婷 严习[1] 沈立明 罗鹏[1,2,3] Zhang Xinglai;Hu Ting;Yan Xi;Shen Liming;Luo Peng(Key Laboratory for Environmental Pollution Monitor and Disease Control,Ministry of Education,Guizhou Medical University,Guiyang 550025,China;Guizhou Provincial Engineering Research Center of Food Nutrition and Health,Guiyang 550025,China;State Key Laboratory of Functions and Applications of Medicinal Plants,Guizhou Medical University,Guiyang 550014,China;Shenzhen Key Laboratory of Marine Biotechnology and Ecology,College of Life Science and Oceanography,Shenzhen University,Shenzhen 518060,China)

机构地区：[1]贵州医科大学公共卫生学院环境污染与疾病监控教育部重点实验室,贵阳550025 [2]贵州省食品营养与健康工程研究中心,贵阳550025 [3]贵州医科大学省部共建药用植物功效与利用国家重点实验室,贵阳550014 [4]深圳大学生命科学与海洋学学院海洋生物技术与生态深圳重点实验室,深圳518060

出　　处：《中华地方病学杂志》2023年第1期4-10,共7页Chinese Journal of Endemiology

基　　金：国家自然科学基金(U1812403-6-2-4、82173642);贵州省教育厅青年科技人才成长项目(黔教合KY字[2022]218)。

摘　　要：目的探讨竹荪多糖对亚砷酸钠诱导大鼠神经毒性的保护作用。方法选择60只SD大鼠(雌雄各半),适应性喂养1周后,采用随机数字表法将大鼠按体质量(80~100 g)分为对照组(n=20,普通饲料)和建模组[n=40,含砷饲料(50 mg/kg亚砷酸钠)]喂养12周后,检测大鼠脑砷与血砷含量(n=10),进行砷中毒模型鉴定;成功建模后,将建模组大鼠分为竹荪多糖组(含砷饲料+20 ml·kg^(-1)·bw竹荪多糖溶液灌胃)、模型组(含砷饲料+等体积蒸馏水灌胃),同时保留对照组(普通饲料+等体积蒸馏水灌胃),每组10只,干预4周。采用Morris水迷宫实验评估大鼠空间学习和记忆能力,尼氏染色观察脑组织病理变化,并测定各组大鼠脑组织中氧化应激因子[超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)]及炎性细胞因子[肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)]水平。结果建模组大鼠的脑砷[(92.02±13.37)μg/g]和血砷含量[(51.37±19.33)μg/L]均高于对照组[(7.42±3.21)μg/g、(2.74±1.29)μg/L,t=-6.91、-6.06,均P<0.001],砷中毒大鼠模型建立成功。与对照组比较,模型组大鼠第1、3、4天逃逸潜伏期和第1次到达时间延长、穿越平台次数减少、目标象限停留时间占比降低(均P<0.05);与模型组比较,竹荪多糖组大鼠第4天逃逸潜伏期和第1次到达时间缩短、目标象限停留时间占比升高(均P<0.05)。尼氏染色可见,与对照组比较,模型组大鼠脑组织尼氏小体数量减少,细胞间隙增大、排列杂乱无章;与模型组比较,竹荪多糖组大鼠脑组织尼氏小体数量增多,大部分神经元结构完整。与对照组比较,模型组大鼠脑组织SOD、GSH-Px水平均较低,MDA、TNF-α、IL-1β水平均较高(均P<0.05);与模型组比较,竹荪多糖组大鼠脑组织SOD、GSH-Px水平均较高,MDA、TNF-α、IL-1β水平均较低(均P<0.05);且竹荪多糖组大鼠脑组织SOD、GSH-Px、MDA、IL-1β水平与对照组比较,差异均无�Objective To investigate the protective effect of Dictyophora polysaccharide on neurotoxicity induced by sodium arsenite in rats.Methods Sixty SD rats(half males and half females)were selected and fed adaptively for one week.The rats were divided into a normal group(n=20,ordinary feed)and a modeling group[n=40,arsenic-containing feed(50 mg/kg sodium arsenite)]according to their body weight(80-100 g)by random number table method.After 12 weeks,the arsenic content in brain and blood of the rats(n=10)was measured to identify the arsenism model.After successful modeling,the rats in the modeling group were divided into Dictyophora polysaccharide group(arsenic-containing feed+20 ml·kg^(-1)·bw Dictyophora polysaccharide solution by gavage),and model group(arsenic-containing feed+equal volume distilled water by gavage),while the rats in the normal group(ordinary feed+equal volume distilled water by gavage)were retained,with 10 rats in each group for 4 weeks of intervention.Morris water maze test was used to assess the spatial learning and memory ability of the rats.Nissl staining was used to observe the pathological changes of the brain tissue,and the oxidative stress factors[superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),malondialdehyde(MDA)],and inflammatory cytokines[tumor necrosis factor-α(TNF-α)and interleukin-1β(IL-1β)]in the brain tissue of each group were measured.Results Brain arsenic content of rats in the modeling group[(92.02±13.37)μg/g]and blood arsenic content[(51.37±19.33)μg/L]were higher than those of the normal group[(7.42±3.21)μg/g and(2.74±1.29)μg/L,t=-6.91,-6.06,P<0.001].The rat model of arsenic poisoning was successfully established.Compared with the normal group,the escape latency on the 1st,3rd and 4th day and the first arrival time of rats in the model group were prolonged,the number of platform crossings was reduced,and the proportion of target quadrant residence time was decreased(P<0.05).Compared with the model group,the escape latency on the 4th day and the first arriva

关 键 词：亚砷酸盐类 竹荪多糖 大脑 氧化应激 炎症反应 

分 类 号：X171.5[环境科学与工程—环境科学]