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作 者:彭静[1]
机构地区:[1]乐山职业技术学院康复基础教研室,四川乐山614000
出 处:《中国药房》2016年第16期2233-2235,共3页China Pharmacy
摘 要:目的:研究丁酸钠对慢性应激模型大鼠空间学习和记忆能力的影响。方法:将SD大鼠随机分为对照组(生理盐水)、模型组(生理盐水)和丁酸钠低、中、高剂量组(50、100、200 mg/kg),每组14只。模型组和丁酸钠各剂量组大鼠给予21 d电击足底刺激,每日1次,每次2 h,以复制慢性应激模型;在刺激前0.5 h ip相应药物。采用Morris水迷宫试验测试各组大鼠的空间学习记忆能力(以逃避潜伏期为指标,连续测试5 d);Western blot法检测海马组织中乙酰化组蛋白H3(ac H3)、ac H4、磷酸化环磷酸腺苷(c AMP)反应元件结合蛋白(p-CREB)、脑源性神经营养因子(BDNF)的表达情况。结果:与对照组比较,模型组和丁酸钠各剂量组大鼠在测试第2天开始逃避潜伏期明显延长(P<0.05),ac H3、ac H4、p-CREB、BDNF表达均降低(P<0.05)。与模型组比较,丁酸钠各剂量组大鼠的逃避潜伏期缩短,其中高剂量组最明显(测试第2天开始差异有统计学意义)(P<0.05);ac H3、ac H4、p-CREB、BDNF表达均增强(P<0.05)。结论:丁酸钠可改善慢性应激造成的大鼠空间学习记忆能力下降,其机制可能是通过恢复大鼠海马区域的组蛋白乙酰化水平,进而上调认知相关蛋白p-CREB、BDNF的表达来实现。OBJECTIVE:To study the effects of sodium butyrate on spatial learning and memory ability in chronic stress model rats.METHODS:SD rats were randomly divided into control group(normal saline),model group(normal saline)and sodium butyrate low-dose,medium-dose and high-dose groups(50,100,200 mg/kg)with 14 rats in each group.Model group and sodium butyrate groups received plantar stimulation by electric shock for 21 d,once a day,2 h each time,to induce chronic stress model.They were given relevant medicine ip 0.5 h before stimulation.Morris water maze test was adopted to test spatial learning and memory ability of rats(using escape latency as index,for consecutive 5 d).Western blot assay was used to detect the expression of ac H3,ac H4,c AMP,p-CREB and BDNF in hippocampus.RESULTS:Compared with control group,escape latency of model group and sodium butyrate groups prolonged significantly on the second day(P〈0.05),and the expression of ac H3,ac H4,p-CREB and BDNF decreased(P〈0.05).Compared with model group,escape latency of sodium butyrate groups shortened,especially in high-dose group(there was statistical significance on the second day of test)(P〈0.05);the expression of ac H3,ac H4,p-CREB,and BDNF enhanced(P〈0.05).CONCLUSIONS:Sodium butyrate can improve chronic stress-induced the decrease of spatial learning and memory ability,the mechanism of which may be recovering histone acetylation level of chronic stress rat hippocampus,and increasing cognitive related proteins such as p-CREB and BDNF.
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