目的 研究锁阳乙酸乙酯部位提取物对去卵巢所致痴呆大鼠的影响及可能的相关机制。方法 SD大鼠50只,随机分为正常组、模型组、假手术组、阳性药组、锁阳乙酸乙酯给药组。采用双侧去卵巢造成大鼠老年痴呆模型,采用Morris水迷宫观察大鼠学习记忆能力的改变, HE染色观察海马部位神经元形态学改变,Western blot 检测磷酸化p38、p-环磷酸腺苷反应元件结合蛋白的表达。结果 锁阳乙酸乙酯给药组的潜伏路程、第一次穿越平台时间较模型组有明显改善。染色结果显示,锁阳给药组可显著改善海马CA1区锥体细胞形态,使之排列整齐、均一、结构清晰;Western blot检测中,p-环磷酸腺苷反应元件结合蛋白表达,在给药组和模型型组之间有显著性差异。结论 锁阳乙酸乙酯部位可显著改善去势大鼠学习记忆能力,可能与调节p38,p-环磷酸腺苷反应元件结合蛋白的表达水平密切相关。
Abstract
OBJECTIVE To study the effect of ethyl acetate extract of Songaricum Rupron(ECS) on ovariectomization induced learning and memory disorder in rats and its potential mechanism. METHODS SD rats were ovariectomized to establish animal model of learning and memory disorder,and taken ECS by intragastric administration(3.3 mg·kg-1). Morris water maze was used to test the learning and memory ability of rats. HE staining was used to observe morphological change of hippocampal neurons. The p38 and p-CREB expression were tested by Western-Blot. RESULTS The latent route of OVX+ECS group in the Morris water maze was significantly shorten, while numbers of crossing platform were markedly increased, compared with OVX group. The neurological form of pyramidal cells in hippocampus were improved by HE staining. CONCLUSION It shows that the p38 expression is reduced while p-CREB is increased in OVX+ECS group, which potentially contributes to the improvement of learning and memory disorder due to lack of endogenous estrogen.
关键词
锁阳 /
去卵巢痴呆 /
学习记忆 /
p-环磷酸腺苷反应元件结合蛋白
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Key words
Cynomorium songaricum /
OVX /
learning /
CREB
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中图分类号:
R965
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参考文献
LU Y, WANG Q, MELZIG M F, et al. Extracts of Cynomorium songaricum protect human neuroblastoma cells from beta-amyloid25-35 and superoxide anion induced injury . Pharmazie, 2009, 64(9):609-612.
LU Y, CHENG F F,WANG X Q, et al. Antioxidant activities of different extracts of Cynomorium songaricum and their protective effects against hypoxanthine /xanthine oxidase-induced cell injury: a comparative study. J Anhui Tradit Chin Med Coll(安徽中医药大学学报),2012,31(4):57-60.
TIAN F Z,CHANG H S. Research on Ovariectomized Rat Model of Alzheimer's Disease.Mod Tradit Chin Med Mater Med-World Sci Technol(世界科学技术-中医药现代化).2014.16(6):1406-1410.
TIAN X M, WANG M F, ZHANG T, et al. The effect of Cynomorium on NO, NOS and bcl-2, bax gene expression in D-galactose aging mice model brain. Chin J Gerontol(中国老年学杂志).2005,25(4):446-447.
JEO S H, LIM Y S, BAE C D, et al. Activation of JNK and p38 in rat hippocampus after kainic acid induced seizure. Exp Mol Med, 2001, 32(4):227-230.
HUANG Y, SHI W, LV H L. The signal pathway of cell DNA damage response of mitogen activated protein kinas. Foreign Med (Physiol, Pathol Clin Med)(国外医学:生理、病理科学与临床分册), 2004, 24(5):438-441.
ZHANG C F, PENG D Y. MAPK cascade signaling and long-term potentiation. Chin Pharmacol Bull(中国药理学通报), 2006, 22(7):769-774.
OTTH C, MENDOZA-NARANJO A, MUJICAL L, et al. Modulation of the JNK and p38 pathways by cdk5 protein kinase in a transgenic mouse model of Alzheimer′s disease. Neuroreport, 2003, 14(18):2403-2409.
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脚注
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基金
国家自然科学基金资助项目(81102622);教育部博士点新教师基金(20110013120004)
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