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蛋白\n>>\n由mAChR\n信号通路\n>>\n神经信号通路\n>>\nmAChR\n天然产物\n>>\n生物碱\n研究领域\n>>\n神经疾病",{"key":236,"value":237},"靶点","5-HT3 Receptor:2.09 μM (IC50)\nmAChR",{"key":239,"value":240},"体外研究","东莨菪碱在表达5-HT3受体的卵母细胞中的应用在单独施用时不引起反应,但在共同施用2μM5-HT期间引起浓度依赖性的反应抑制。东莨菪碱的pIC50值为5.68±0.05(IC50 =2.09μM,n = 6),Hill斜率为1.06±0.05。这得到Kb为3.23μM。当在5-HT应用期间施用东莨菪碱时也观察到相同的浓度依赖性效应。为了进一步测试5-HT3受体的竞争性结合,用[3H]格拉司琼测量未标记的东莨菪碱的竞争,[3H]格拉司琼是这些受体上已建立的高亲和力竞争性拮抗剂。东莨菪碱与0.6 nM [3H]格拉司琼(~Kd)显示浓度依赖性竞争,平均pKi为5.17±0.24(Ki =6.76μM,n = 3)[1]。",{"key":242,"value":243},"体内研究","在组织病理学研究中,大脑的组织学没有显着变化。然而,观察到用仅接受蒸馏水的东莨菪碱预处理的对照小鼠的海马细胞密度降低[2]。与正常组(3.06±0.296)相比,单独使用东莨菪碱可显着提高乙酰胆碱酯酶(AchE)的活性(7.98±0.065; P \u003C0.001)。与正常组(12.82±2.86)相比,用东莨菪碱治疗的动物报告丙二醛(MDA)水平显着增加(34.61±4.85; P \u003C0.01)。与正常组(0.3906±0.02)相比,东莨菪碱处理组显示还原型谷胱甘肽(GSH)水平显着降低(P \u003C0.001; 0.1504±0.03)。与正常组(43.21±3.46)相比,东莨菪碱治疗的大鼠显示β淀粉样蛋白(Aβ1-42)浓度显着增加(P \u003C0.001; 146.2±1.74)[3]。",{"key":245,"value":246},"激酶实验","通过将稳定表达5-HT3受体的HEK 293细胞的粗提取物或豚鼠膜制剂在含有10mM HEPES缓冲液（pH7.4）和0.1-1nM的0.5mL培养物中孵育来测量饱和结合（8点）曲线。 3H]格拉司琼或1-10nM [3H] N-甲基 - 环丙胺。通过在含有0.6nM [3H]格拉司琼或0.6nM [3H] N-甲基环丙胺和不同浓度的竞争配体的0.5mL HEPES缓冲液中孵育相同的受体制剂来测定竞争结合（10分）。用1mM喹哌啶或10μM东莨菪碱分别测定非特异性结合。通过过滤到用HEPES缓冲液+ 0.3％聚乙烯亚胺润湿的Whatman GF \u002F B过滤器终止孵育，然后用冰冷的HEPES缓冲液快速洗涤两次。使用具有牛血清白蛋白标准品的Lowry蛋白质测定法计算蛋白质浓度。使用Tri-Carb 2100 TR闪烁计数器[1]测量放射性。",{"key":248,"value":249},"动物实验","小鼠[2]将小鼠称重，标记并分成7组，每组5只动物，之后所有动物腹膜内预先注射3mg \u002F kg东莨菪碱。第1-3组给予0.2mL等效剂量的4mg \u002F kg，6mg \u002F kg和8mg \u002F kg的巴戟天提取物，而4-6组给予相同剂量的紫穗槐提取物，第7组给予0.2。连续3天蒸馏水（阴性对照）。大鼠[3]在该研究中使用重180-200g的健康雄性Wistar大鼠（12个月大）。将大鼠分成5组（n = 6 \u002F组）;组I-正常对照，组II-疾病对照（氢溴酸东莨菪碱3mg \u002F kg，ip），组III-东莨菪碱+槲皮素（25mg \u002F kg，po），组IV-标准治疗（东莨菪碱+盐酸多奈哌齐3mg \u002F kg，po）和V-东莨菪碱+槲皮素（25mg \u002F kg，口服）+多奈哌齐（3mg \u002F kg，口服）。 III组，IV组和V组大鼠每24小时间隔给药各自的药物连续14天。 Morris水迷宫，高架迷宫和被动回避范例的采集路线在第14天进行，东莨菪碱（3 mg \u002F kg，ip）在采集后第14天给予除正常对照外的所有组引起大鼠认知障碍的群体。在第15天测试记忆保留，并在同一天，处死大鼠并分离脑组织以估计乙酰胆碱酯酶（AchE）和脑氧化应激标记物如脂质过氧化物酶（LPO），谷胱甘肽（GSH）（减少） ）。 ELISA试剂盒用于估计β淀粉样蛋白（Aβ1-42）水平。解剖出大鼠的海马体并研究其组织病理学变化。",{"key":251,"value":252},"参考文献","[1].\nLochner M, et al. The muscarinic antagonists Scopolamine and atropine are competitive antagonists at 5-HT3 receptors. Neuropharmacology. 2016 Sep;108:220-8.\n[2].\nO ET, et al. COGNITIVE-ENHANCING PROPERTIES OF MORINDA LUCIDA (RUBIACEAE) AND PELTOPHORUM PTEROCARPUM (FABACEAE) IN SCOPOLAMINE-INDUCED AMNESIC MICE. Afr J Tradit Complement Altern Med. 2017 Mar 1;14(3):136-141.\n[3].\nPattanashetti LA, et al. Evaluation of neuroprotective effect of Quercetin with Donepezil in Scopolamine-induced amnesia in rats. 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