金钗石斛多糖减轻脂多糖诱导的大鼠学习记忆减退及机制研究  

Dendrobium Nobile Polysaccharides Attenuate Learning and Memory Deficits Induced by Lipopolysaccharide in Rats

作　　者：王丽娜[1] 龚其海[1] 李菲[1] 吴芹[1] 石京山[1] 

机构地区：[1]遵义医学院基础药理省部共建教育部重点实验室暨药理学教研室

出　　处：《神经药理学报》2016年第1期1-8,共8页Acta Neuropharmacologica

基　　金：国家自然科学基金项目(No.30960447);教育部创新团队项目(No.IRT1197);贵州省科技厅联合基金项目(黔科合J字LKZ[2012]43号)

摘　　要：目的:观察金钗石斛多糖(Dendrobium nobile polysaccharides,DNP)对脂多糖(lipopolysaccharide,LPS)诱导的大鼠学习记忆减退及神经炎症的改善作用。方法:DNP(40、80、160 mg·kg-1·d-1)预防性给药7 d,侧脑室注射20μg LPS制备大鼠学习记忆减退模型。制模后d 5开始,Morris水迷宫法检测大鼠的空间辨别学习记忆能力。行为学检测结束后,HE染色观察大鼠海马神经元的细胞形态改变,RT-PCR及Western Blot分别检测大鼠海马组织中肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)、白介素1β(interleukine-1β,IL-1β)、转化生长因子β1(transforming growth factor-β1,TGF-β1)的m RNA及蛋白表达。结果:与假手术组比较,模型组大鼠在定位航行实验中逃避潜伏期明显延长,在空间探索实验中其校正潜伏期明显缩短;大鼠海马神经元排列散乱,部分神经元丢失,出现核固缩,嗜伊红染色;大鼠海马组织中TNF-α、IL-1β、TGF-β1 m RNA及其蛋白的表达量明显增加。DNP(40、80、160 mg·kg-1·d-1)给药组能改善大鼠学习记忆能力,对抗LPS引起的大鼠海马CA1区神经元损伤,并降低大鼠海马组织中TNF-α、IL-1β、TGF-β1的m RNA及蛋白表达。结论:DNP可减轻LPS诱导的大鼠学习记忆减退及神经元损伤,抑制其海马的炎症反应。Objective：To investigate the protective effects and potential mechanisms ofDendrobium nobile polysaccharides（DNP） fromDendrobium nobileLindl. on learning and memory deficits induced by lipopolysaccharide（LPS）.Methods：Rats were orally treated with DNP（40,80,160 mg·kg-1） for 7 days,followed by bilateral intra-cerebroventricular injection of LPS（20μg·rat-1） to induce learning and memory deficits. Rats were continued to receive DNP until the end of experiments. Morris water maze was used to test the abilities of spatial learning and memory. The neuronal injury in hippocampus was observed by hematoxylin-eosin staining. The mRNA and protein expressions of neuroinflammation-related genes and proteins in rats hippocampus were detected by real time RT-PCR and Western blot,respectively.Results：Compared to sham（saline-injected） rats,LPS significantly prolonged the escape latency in the navigation test and shortened the adjusted escape latency（P〈0.01）. These learning and memory deficits were significantly improved by DNP treatment（P〈0.01）. LPS injection caused neuronal injury in hippocampus,and increased the mRNA and protein expressions of TNF-α,IL-1β and TGF-β1 in rat hippocampus（P〈0.01）,which were suppressed by DNP treatments（P〈0.05）. Conclusions：DNP could protect LPS-induced learning and memory deficits and neuronal injury in rats. The mechanisms appear to be due to the inhibition of LPS-elicited inflammatory responses in the hippocampus.

关 键 词：金钗石斛多糖 脂多糖 学习记忆 炎症因子 

分 类 号：R285.5[医药卫生—中药学]