益智Ⅱ号对记忆保持及消退中海马CA3区突触结构的影响

目的:观察益智II号对小鼠记忆保持及消退过程中海马CA3区突触结构的影响。方法:给小鼠灌胃益智II号口服液0.2ml.d-1,连续20d。给药结束后,进行一次性被动回避反应训练,24h后检测小鼠记忆的保持。在行为训练前及训练后的第6d、第12d分别取海马CA3区,电镜观察不同时期突触结构的变化。结果:①在行为训练后的第1d、第6和第12d,益智II号组动物的步入潜伏期明显长于对照组(P<0.01,P<0.05);②行为训练后的第6、第12d,不论是对照组还是益智II号组,海马CA3区突触活性区长度均显著大于行为训练前(P<0.01,P<0.05);在行为训练后的同一时期,益智II号组的突触活性区长度明显大于对照组(P<0.01);③在行为训练后的第6d,益智II号组中轴树突触、穿孔突触的数量明显高于学习前(P<0.05),也高于同一时期对照组动物(P<0.05)。结论:益智II号能明显促进小鼠记忆的保持,延缓记忆消退;益智II号促进记忆保持可能与其增加海马CA3区突触活性区长度、轴树突触及穿孔突触的数量有关。     

补肾活血法对AD模型小鼠行为学的影响

目的:研究中医补肾活血法指导下中药复方(益智健脑方浓缩液)以及针刺("补肾活血针刺法")对阿尔茨海默病模型小鼠SAMP8(Senescgnce Accelerated Mouse P8,SAMP8)的行为学影响,从不同侧面阐明补肾活血法对SAMP8小鼠的治疗作用以及防治AD的可行性.方法:将5月龄雄性SAMP8 30只随机分为中药治疗组(n=10)、针刺治疗组(n=10)和模型对照组(n=10),中药治疗组以益智健脑方浓缩液灌胃;针刺治疗组予以"补肾活血针刺法"干预;模型对照组不予任何处理;另设5月龄雄性SAMR1小鼠(n=10)作为正常对照组.4周后,采用Morris水迷宫对各组小鼠的行为学进行检测分析其学习记忆能力的变化.结果:Morris水迷宫实验中,模型对照组SAMP8小鼠的逃避潜伏期较正常对照组SAMR1小鼠的逃避潜伏期时间明显延长(P<0.05),停留在原平台象限的时间和穿越原平台次数较正常对照组SAMR1小鼠明显减少(P<0.05);补肾活血法指导下,采用中药复方益智健脑方浓缩液以及"补肾活血针刺法"干预均能够明显缩短SAMP8小鼠的逃避潜伏期(P<0.05),增加其停留在原平台象限的时间和穿越原平台次数(P<0.05).结论:补肾活血法能够明显改善AD模型小鼠SAMP8的学习记忆能力以及记忆巩固、再现能力.     

土人参提取液对D-半乳糖所致衰老小鼠的抗氧化作用研究

本文研究了土人参提取液对D-半乳糖所致衰老小鼠的抗氧化作用的影响。取昆明种小白鼠50只,随机分为5组(正常对照组、衰老模型组、土人参提取液低、中、高剂量组)。除正常对照组外,其余各组每天于颈背皮下注射D-半乳糖125 mg/kg,连续42 d,造成亚急性衰老模型。在注射D-半乳糖的同时,三个不同剂量实验组每天分别灌胃土人参提取液5、10和15g/kg,正常对照组及衰老模型组给予等量生理盐水。于42 d后测定小鼠体内超氧化物歧化酶(Super Oxide Dismutase,SOD)、谷胱甘肽过氧化物酶(Glutathione peroxidase,GSH-PX)等酶的活性,及丙二醛(Maleic Dialdehyde,MDA)的含量。结果显示:与正常对照组相比,衰老模型组小鼠心脏、肝脏组织SOD及血清中GSH-PX活性降低(P0.01),MDA含量增加(P0.01)。与衰老模型组相比,土人参提取液低、中、高剂量组小鼠心脏、肝脏组织SOD及血清中GSH-PX活性明显升高(P0.01);中、高剂量组小鼠心脏、肝脏组织中MDA含量降低明显(P0.01),低剂量组小鼠肝脏的MDA含量明显降低(P0.01)。上述结果表明:土人参提取液对D-半乳糖所致衰老小鼠有抗衰老作用。     

藏药小檗皮对糖尿病模型小鼠血糖水平影响的初步研究

目的:观察藏药小檗皮对糖尿病小鼠模型及正常小鼠血糖的影响,并以血糖为指标确定其治疗糖尿病及其并发症的有效剂量范围.方法:以6.72 9·kg-1、3.36 9·kg-1、1.68 g·kg-1、0.84 9·kg-1、0.42 g.· kg-1剂量的小檗皮浸膏灌胃四氧嘧啶糖尿病小鼠10d,GOD-CE-PAP法测定小鼠血糖水平,以确定小檗皮的有效降糖剂量范围;6.72 g·kg-1、1.68 g·kg-1、0.84 g·kg-1剂量的小檗皮浸膏灌胃正常小鼠7d,GOD-CE-PAP法测定小鼠血糖水平,观察小檗皮对正常小鼠血糖的影响.结果:与模型对照组相比,盐酸二甲双胍、盐酸小檗碱、生物碱复配及6.72 g·kg-1、1.68 9·k-1、0.84 9·kg-1、3.36 g·kg-1、0.42 g·kg-1的小檗皮浸膏均有较好的降糖作用,5个剂量的小檗皮浸膏降糖作用依次为:6.72 9·kg-1＞ 1.689·kg-1＞ 0.849·kg-1＞3.36 g·kg-1＞0.429·kg-1;盐酸二甲双胍、羟苯磺酸钙、盐酸小檗碱、复配生物碱及6.72 9·kg-1、1.68 g·kg-1、0.849·kg-1剂量的小檗皮浸膏对正常小鼠血糖无明显作用.结论:藏药小檗皮对四氧嘧啶所致糖尿病模型小鼠血糖有明显降糖作用,对正常小鼠血糖无明显作用.     

MPTP致空间学习记忆障碍小鼠脑内NSF表达变化

目的:观察1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)致空间学习记忆障碍小鼠脑内N-乙基马来酰亚胺敏感融合蛋白(NSF)表达变化。方法:C57BL/6J小鼠随机分为2组(n=24),包括对照组和MPTP处理组,雌雄各半。MPTP处理组给予C57BL/6J小鼠MPTP(20 mg/0.2 ml/(kg·d),s.c.)连续8 d,每天一次,对照组给予等量的生理盐水用同样方法处理。第9天起采用水迷宫实验,连续4 d检测C57BL/6J小鼠空间学习记忆的改变,水迷宫实验测试结束后,采用免疫组化和Western blot方法检测小鼠脑内NSF表达改变。结果:每组选取小鼠24只进行水迷宫测试,与对照组相比,MPTP处理组小鼠出现空间学习记忆障碍;每组选取小鼠5只进行免疫组化检测,同时每组选取5只小鼠进行Western blot检测,海马CA1区NSF免疫反应活性明显减弱(P0.01),前额叶皮层NSF的免疫反应活性(P0.01)和蛋白表达(P0.05)都明显增高。结论:MPTP致空间学习记忆障碍小鼠脑内NSF表达出现异常,可能参与MPTP致空间学习记忆障碍的发病机制。     

姜黄素对APPswe/PS1dE9双转基因小鼠Aβ生成和降解的影响

目的观察姜黄素对APPswe/PS1dE9双转基因小鼠β淀粉样蛋白(βamyloid,Aβ)生成酶早老素2(presenilin2,PS2)和Aβ降解酶胰岛素降解酶(insulin degrading enzyme,IDE)表达的影响,探讨姜黄素在AD防治中的机制。方法将3月龄的APPswe/PS1dE9双转基因小鼠随机分为模型组、阳性对照组[罗格列酮组,0.92mg/(kg·d)]、姜黄素大[400mg/(kg·d)]、中[200mg/(kg·d)]、小[100mg/(kg·d)]剂量组,每组10只;并以同月龄遗传背景相同的C57BL/6J小鼠作为正常对照组10只。每天灌胃给药1次,模型组和正常对照组用等体积0.5%羧甲基纤维素(carboxymethyl cellulose,CMC)灌胃。灌胃3个月后,应用Morris水迷宫、免疫组织化学等方法,检测动物的学习记忆能力、海马Aβ生成酶PS2和降解酶IDE表达变化。结果行为学检测,模型组小鼠的游泳轨迹多为边缘型,而正常对照组、阳性对照组、姜黄素各组小鼠的游泳轨迹多为趋向型和直线型。Aβ生成酶PS2和降解酶IDE的免疫组织化学染色结果,模型组小鼠海马CA1区PS2阳性细胞较正常对照组明显增加(P0.01),与模型组相比,姜黄素各组小鼠海马CA1区PS2阳性细胞减少(P0.01)。模型组小鼠海马CA1区PS2阳性细胞平均灰度值较正常对照组降低(P0.05),姜黄素小剂量组阳性细胞平均灰度值同模型组相比明显增加(P0.01)。模型组小鼠海马CA1区IDE阳性细胞较正常对照组明显减少(P0.01),与模型组相比,姜黄素中剂量组小鼠海马CA1区IDE阳性细胞明显增加(P0.05)。模型组小鼠海马CA1区IDE阳性细胞平均灰度值较正常对照组明显增加(P0.01),姜黄素各组小鼠海马CA1区IDE阳性细胞平均灰度值同模型组相比均明显降低(P0.01)。结论姜黄素能通过减少Aβ生成酶和增加Aβ降解酶的表达,降低Aβ蛋白的表达进而改善APPswe/PS1dE9双转基因小鼠的学习记忆能力。     

金思维对东莨菪碱致记忆障碍小鼠脑胆碱能系统的影响

目的 通过建立东莨菪碱记忆障碍模型,采用中药复方金思维进行干预,观察金思维对东莨菪碱致记忆障碍模型小鼠行为学和胆碱能系统的影响,探讨该药的神经保护作用机制。方法 将ICR小鼠随机分为正常对照组;模型组,溶媒0.5%CMC;阳性对照组,多奈哌齐,0.92 mg/(kg·d);金思维大、中、小剂量组,20、10、5 mg/(kg·d)。每组18只,按0.1 mL/10 g小鼠体重连续灌胃给药30 d。末次给药后造模,对照组腹腔注射生理盐水,其余各组腹腔注射东莨菪碱3 mg/(kg·d),溶于0.9%生理盐水,按0.1 mL/10 g小鼠体重注射,进行Morris水迷宫实验。实验结束后取皮层和海马组织,分别测定皮层和海马中乙酰胆碱(Ach)含量、乙酰胆碱酯酶(Ach E)及胆碱乙酰转移酶(Ch AT)活性。结果 金思维可使模型小鼠游泳距离和游泳时间缩短及目标象限停留时间增长;金思维可使模型组小鼠脑内Ach含量升高、Ach E活性下降和Ch AT活性升高。结论 金思维可以改善东莨菪碱导致的记忆障碍模型小鼠学习记忆能力,其机制可能与胆碱能能系统有关。     

钩藤散改善APP/PS1双转基因小鼠学习记忆功能的代谢组学研究

目的:采用非靶向的高通量尿液代谢组学技术对钩藤散改善淀粉样前体蛋白/早老素蛋白1基因,即APP/PS1双转基因小鼠的作用机制进行研究。方法:5月龄APP/PSI小鼠采用Morris水迷宫实验检测双转基因小鼠的空间学习能力,在确定出现空间记忆能力功能损伤地条件下采用基于非靶向的尿液代谢组学技术研究APP/PSI小鼠的代谢网络,聚焦关键通路,同时观察钩藤散在水迷宫和代谢水平上的治疗作用。结果:Morris水迷宫对比发现APP/PSI小鼠的空间记忆能力明显长于同窝野生小鼠,给予钩藤散后呈现一定程度的回调趋势,经非靶向的代谢轮廓分析和核心代谢通路聚焦后,成功发现正常小鼠(同窝野生小鼠)和APP/PSI双转基因小鼠代谢轮廓间差异最大的信号,经质谱解析和权威数据库检索后鉴定6个与学习记忆相关的潜在生物标记物,分别是牛磺酸(taurine)、叶酸(pteroylglutamic acid)、新蝶呤(neopterin)、磺乙谷酰胺(glutaurine)、戊邻酮二酸盐(2-oxoglutarate)、二氢新蝶呤(dihydroneopterin),他们主要涉及牛磺酸代谢及叶酸代谢等,经钩藤散治疗后能有效回调。结论:钩藤散对APP/PSI双转基因小鼠的学习记忆能力具有一定治疗作用,本次发现的6个生物标记物可能是APP/PSI双转基因小鼠发病的潜在靶点,为钩藤散的相关药效学研究提供实验依据。     

新疆药桑桑叶对2-型糖尿病小鼠血糖和脂质代谢的影响北大核心CSCD

分析新疆药桑桑叶水提物和生物碱浸膏对试验性2-型糖尿病小鼠血糖和脂质代谢的影响。采用高脂高糖饲料加链脲佐菌素诱导糖尿病小鼠模型,根据体质量、血糖水平将小鼠随机分为9组:即对照组、模型组、罗格列酮(阳性药物)组、桑叶水提物高(AE-HD)、中(AE-MD)、低(AE-LD)剂量组和生物碱浸膏高(TA-HD)、中(TA-MD)、低(TA-LD)剂量组,每组10只。连续灌胃给药30 d,观察小鼠血糖、血脂、胰岛素水平、糖耐量及氧化应激指标的变化。与模型组相比,桑叶水提物组和生物碱浸膏组均能够显著降低糖尿病小鼠的空腹血糖(P<0.05,P<0.01),显著提高血清胰岛素水平(P<0.01),而且显著降低2-型糖尿病小鼠的LDL和TG,增加对胰岛素的敏感性(P<0.01),使小鼠血清SOD活力显著升高(P<0.01),MDA水平明显下降;糖耐量试验中,桑叶水提物组和生物碱浸膏组在0.5 h、1 h和2 h测得的血糖值与模型组相比均呈现极显著性差异(P<0.01)。表明新疆药桑桑叶水提物和生物碱浸膏均具有一定的降血糖作用,且桑叶水提物优于生物碱浸膏,同时能有效改善糖尿病小鼠脂质代谢紊乱,增强活性氧清除能力,并提高糖尿病小鼠糖耐量。     

新疆药桑桑叶对2-型糖尿病小鼠血糖和脂质代谢的影响

分析新疆药桑桑叶水提物和生物碱浸膏对试验性2-型糖尿病小鼠血糖和脂质代谢的影响。采用高脂高糖饲料加链脲佐菌素诱导糖尿病小鼠模型,根据体质量、血糖水平将小鼠随机分为9组:即对照组、模型组、罗格列酮(阳性药物)组、桑叶水提物高(AE-HD)、中(AE-MD)、低(AE-LD)剂量组和生物碱浸膏高(TA-HD)、中(TA-MD)、低(TA-LD)剂量组,每组10只。连续灌胃给药30 d,观察小鼠血糖、血脂、胰岛素水平、糖耐量及氧化应激指标的变化。与模型组相比,桑叶水提物组和生物碱浸膏组均能够显著降低糖尿病小鼠的空腹血糖(P0.05,P0.01),显著提高血清胰岛素水平(P0.01),而且显著降低2-型糖尿病小鼠的LDL和TG,增加对胰岛素的敏感性(P0.01),使小鼠血清SOD活力显著升高(P0.01),MDA水平明显下降;糖耐量试验中,桑叶水提物组和生物碱浸膏组在0.5 h、1 h和2 h测得的血糖值与模型组相比均呈现极显著性差异(P0.01)。表明新疆药桑桑叶水提物和生物碱浸膏均具有一定的降血糖作用,且桑叶水提物优于生物碱浸膏,同时能有效改善糖尿病小鼠脂质代谢紊乱,增强活性氧清除能力,并提高糖尿病小鼠糖耐量。     

Evaluation of nootropic potential of Ocimum sanctum Linn. in mice

Dementia is one of the age related mental problems and a characteristic symptom of various neurodegenerative disorders including Alzheimer's disease. Certain drugs like diazepam, barbiturates and alcohol disrupt learning and memory in animals and man. However, a new class of drugs known as nootropic agents is now used in situations where there is organic disorder in learning abilities. The present work was undertaken to assess the potential of O. sanctum extract as a nootropic and anti-amnesic agent in mice. Aqueous extract of dried whole plant of O. sanctum ameliorated the amnesic effect of scopolamine (0.4 mg/kg), diazepam (1 mg/kg) and aging induced memory deficits in mice. Elevated plus maze and passive avoidance paradigm served as the exteroceptive behavioral models. O. sanctum extract decreased transfer latency and increased step down latency, when compared to control (piracetam treated), scopolamine and aged groups of mice significantly. O. sanctum preparations could of beneficial in the treatment of cognitive disorders such as dementia and Alzheimer's disease.     

川芎嗪对痴呆小鼠模型学习记忆能力的影响

目的研究川芎嗪对痴呆小鼠学习记忆的影响。方法对APPswe/PSΔE9双转基因小鼠在3月龄开始食物中连续给川芎嗪（100 mg/kg.d）进行治疗,停药后立即进行水迷宫实验,并与未给药APPswe/PSΔE9双转基因小鼠和及野生鼠进行比较。结果治疗组与APPswe/PSΔE9双转基因组比较,平台寻找潜伏期缩短,穿过原平台区的频次增加。结论川芎嗪能改善APPswe/PSΔE9痴呆模型小鼠的学习记忆能力。     

中药麝香胶囊抑瘤作用的实验研究

目的探讨中药麝香胶囊对小鼠实验性肿瘤的疗效。方法昆明小鼠分别接种艾氏腹水癌、S-180、肝癌细胞株（hepatocellular carcinoma,HCC）三种癌细胞株,接种24h后开始给予中药麝香胶囊,每日1次,共10d。分高、中、低三个剂量给药（4、2、1g／kg以主药麝香药量计）。阳性对照以天仙丸胶囊（1g／kg）一次性灌服。阴性对照组以同体积生理盐水灌服。接种实体瘤动物于第10天处死,称瘤重,计算抑瘤率;接种腹水瘤动物,观察存活时间,计算生命延长率。结果中药麝香胶囊对实体癌有一定的抑瘤作用,但未达到药典规定的抑瘤率30％的要求;对腹水癌也有一定的抑瘤作用,但也未达到药典规定生命延长率50％的要求;统计学分析（P〉0．05）差异没有显著性。结论中药麝香胶囊抑瘤作用不明显,其配方及剂型有待进一步研究与改进。     

中药银杏叶对老年痴呆症小鼠学习记忆能力的影响

目的研究中药银杏叶与西药脑复康片对老年痴呆症小鼠学习记忆能力恢复效果的差异。方法 KM小鼠随机分为对照组、模型组、银杏叶组和脑复康组,各组20只。除对照组外,其余组采用腹腔注射D-半乳糖和灌胃AlCl3进行造模,连续60 d。银杏叶组和脑复康组自造模起给予相应的药物,连续60 d。试验结束后测定小鼠学习记忆能力,测定脑组织中乙酰胆碱酯酶活性、过氧化脂质（MDA）含量、超氧化岐化酶（SOD）活性、Na＋、K＋-ATPase、游离钙离子含量和进行脑神经元细胞计数。结果与模型组比较,银杏叶组动物潜伏期明显延长,错误次数降低（P〈0.05）;银杏叶组动物脑组织SOD活性明显升高（P〈0.05）,MDA含量、Ca＋浓度含量、乙酰胆碱酯酶活性显著性降低（P〈0.05）,与对照及脑复康组比较未见显著差异（P〉0.05）;银杏叶组动物大脑海马锥体细胞数与模型组比较明显升高（P〈0.01）,大脑皮质神经元细胞数与模型组比较无明显差异（P〉0.05）。结论中药银杏叶改善小鼠学习记忆障碍的作用与西药脑复康片相似。     

Chrysophanol Relieves Cognition Deficits and Neuronal Loss Through Inhibition of Inflammation in Diabetic Mice

Patients with diabetes mellitus are easy to experience diabetic encephalopathy (DE) and other cognition dysfunction, whereas the neural alterations in developing this disease are unknown yet. Chrysophanol (CHR) is one of traditional Chinese medicine which was reported to show protective effects in cognition dysfunction and inflammatory in previously studies. In this current study, whether CHR protects learning and memory dysfunctions induced by diabetes disease or not and underlying mechanisms were studied. DE model was induced by streptozotocin (STZ, i.p.) in ICR mice. CHR was administrated 3 days after STZ treated mice which was confirmed with diabetes for consecutive 6 days. Learning and memory function was tested by Morris water maze after the CHR injection. The morphology of neuronal cells in hippocampus CA3 region was stained by HE-staining. ELISA and Western blot assay were used to determine the levels of pro-inflammation cytokines (IL-1β, IL-4, IL-6, TNF-α) in hippocampus. Here, we demonstrated that mice harboring diabetes mellitus induced by STZ exhibit high blood glucose, learning and memory deficits detected by Morris water maze behavior tests. Application with CHR right after developing diabetes disease rescues partial blood sugar increasing, learning and memory deficits. The data also indicated that the death rate of neurons and the number of astrocytes in hippocampus CA3 region was significantly improved in diabetic mice. Moreover, the underlying mechanisms of CHR’s protective effect are likely associated with anti-inflammation by downregulating the expression of pro-inflammation cytokines (IL-1β, IL-4, IL-6, TNF-α) in hippocampus and inhibiting the over-activation of astrocytes in hippocampus CA3 region. Therefore, application with CHR contributes to the learning and memory deficits induced by diabetes disease via inhibitory expressions of inflammatory in hippocampus region.     

四君子汤及其纳米制剂对微生态失调小鼠的调整作用

目的研究四君子汤水提液及纳米制剂对肠道微生态失调小鼠的调整作用。方法应用林可霉素灌胃建立小鼠肠道微生态失调模型,然后应用四君子汤水提液(常态中药)及其纳米制剂进行治疗,同时设正常、阳性对照及自然恢复组,于给药6 d后处死小鼠,进行肠道菌群检测、肠组织电镜检查及肝脏细菌易位检测。结果林可霉素灌胃3 d后,小鼠肠道菌群失调,肠黏膜损伤严重,肝脏有大量细菌易位。持续6 d治疗后,肠道双歧杆菌和乳酸杆菌菌量明显上升,损伤的肠黏膜基本修复,肝脏细菌易位数量大幅度下降。各治疗组间比较纳米中药组的效果要好于常态中药和丽珠肠乐组(P<0.001,P<0.01,P<0.05)。结论2种不同粒径的中药均能扶植肠道正常菌群生长,促进肠黏膜损伤修复,控制细菌易位。但纳米中药效果优于常态中药,且用药量小。     

Qingyangshen mitigates amyloid-β and Tau aggregate defects involving PPARα-TFEB activation in transgenic mice of Alzheimer's disease

BackgroundAlzheimer's disease (AD) is the most common neurodegenerative disease. Deposition of amyloid β plaques (Aβ) and neurofibrillary tangles (NFTs) is the key pathological hallmark of AD. Accumulating evidence suggest that impairment of autophagy-lysosomal pathway (ALP) plays key roles in AD pathology.PurposeThe present study aims to assess the neuroprotective effects of Qingyangshen (QYS), a Chinese herbal medicine, in AD cellular and animal models and to determine its underlying mechanisms involving ALP regulation.MethodsQYS extract was prepared and its chemical components were characterized by LC/MS. Then the pharmacokinetics and acute toxicity of QYS extract were evaluated. The neuroprotective effects of QYS extract were determined in 3XTg AD mice, by using a series of behavioral tests and biochemical assays, and the mechanisms were examined in vitro.ResultsOral administration of QYS extract improved learning and spatial memory, reduced carboxy-terminal fragments (CTFs), amyloid precursor protein (APP), Aβ and Tau aggregates, and inhibited microgliosis and astrocytosis in the brains of 3XTg mice. Mechanistically, QYS extract increased the expression of PPARα and TFEB, and promoted ALP both in vivo and in vitro.ConclusionQYS attenuates AD pathology, and improves cognitive function in 3XTg mice, which may be mediated by activation of PPARα-TFEB pathway and the subsequent ALP enhancement. Therefore, QYS may be a promising herbal material for further anti-AD drug discovery.     

Neuroprotective effects of quercetin, rutin and okra (Abelmoschus esculentus Linn.) in dexamethasone-treated mice

The administration of dexamethasone, a synthetic glucocorticoid receptor agonist, causes neuronal death in the CA3 layer of the hippocampus, which has been associated with learning and memory impairments. This study aimed to examine the ability of okra (Abelmoschus esculentus Linn.) extract and its derivatives (quercetin and rutin) to protect neuronal function and improve learning and memory deficits in mice subjected to dexamethasone treatment. Learning and memory functions in mice were examined using the Morris water maze test. The results showed that the mice treated with dexamethasone had prolonged water maze performance latencies and shorter time spent in the target quadrant while mice pretreated with quercetin, rutin or okra extract prior to dexamethasone treatment showed shorter latencies and longer time spent in target quadrant. Morphological changes in pyramidal neurons were observed in the dexamethasone treated group. The number of CA3 hippocampal neurons was significantly lower while pretreated with quercetin, rutin or okra attenuated this change. Prolonged treatment with dexamethasone altered NMDA receptor expression in the hippocampus. Pretreatment with quercetin, rutin or okra extract prevented the reduction in NMDA receptor expression. Dentate gyrus (DG) cell proliferation was examined using the 5-bromo-2-deoxyuridine (BrdU) immunohistochemistry technique. The number of BrdU-immunopositive cells was significantly reduced in dexamethasone-treated mice compared to control mice. Pretreatment with okra extract, either quercetin or rutin was found to restore BrdU-immunoreactivity in the dentate gyrus. These findings suggest that quercetin, rutin and okra extract treatments reversed cognitive deficits, including impaired dentate gyrus (DG) cell proliferation, and protected against morphological changes in the CA3 region in dexamethasone-treated mice. The precise mechanism of the neuroprotective effect of these plant extracts should be further investigated.     

应用单分子荧光成像技术研究人参抗运动性疲劳分子机制

采用单分子荧光成像技术,通过建立运动性疲劳的细胞模型对中药人参抗运动性疲劳的分子机制进行研究。取新生大鼠骨骼肌细胞,将其随机分成人参组和对照组。在两组细胞的培养基中分别加入2mg／mL人参提取物和等量的D—hanks液进行培养。两组细胞分化成肌管后,将用钙离子染料处理过的细胞置于共聚焦显微镜上检测其荧光强度。待荧光强度稳定时,分别向两组细胞加1μmol／L地塞米松溶液,记录并比较两组细胞用地塞米松刺激前后荧光强度的改变幅度。结果发现,两组细胞胞浆内钙离子的荧光强度均明显增强（P〈0．05）,但人参提取物组细胞胞浆内钙离子浓度的增加幅度明显低于对照组（P〈0．05）。由此可见,人参提取物对地塞米松刺激引起的疲劳骨骼肌细胞具有保护作用,人参消除运动性疲劳的机制可能与其调节骨骼肌细胞胞浆内钙离子浓度有关。     

藏波罗花提取物对小鼠耐缺氧作用的研究

采用不同方法建立小鼠常压缺氧模型、亚硝酸钠中毒模型及急性脑缺血性缺氧模型,对藏波罗花提取物的耐缺氧活性进行研究。以0.5%羧甲基纤维素钠溶液为空白对照、盐酸普萘洛尔为阳性对照药,设置藏波罗花60%乙醇提取物、95%乙醇提取物的5g/kg、10g/kg、15g/kg三个剂量的给药组,通过观察小鼠存活时间,研究藏波罗花提取物对小鼠缺氧损伤的保护作用。结果显示,与空白对照组相比较,藏波罗花提取物各剂量组均能明显延长小鼠在常压缺氧、亚硝酸钠中毒及急性脑缺血性缺氧条件下的存活时间(P<0.05),表明藏波罗花提取物具有一定的耐缺氧活性,可提高实验小鼠的耐缺氧能力。