Effects of Longyanshen polysaccharides on free radical metabolism in senescence accelerated-prone mice

BACKGROUND： Along with aging, antioxidase activity decreases and oxygen-derived free radicals greatly accumulate, resulting in cellular senescence, or even cell death. This is manifested by hypomnesia and disordered metabolism of free radicals. Studies have reported that Longyanshen polysaccharides have the function of antioxidation and improved brain memory. OBJECTIVE： To observe the effects of Longyanshen polysaccharides on free radical metabolism in brain tissue to verify the anti-aging mechanisms in senescence accelerated-prone （SAMP8） mice. DESIGN, TIME AND SETTING： The randomized, controlled, biochemical experiment was performed in the Department of Pharmacology and Scientific Experimental Center of Guangxi Medical University （China） from September 2005 to January 2008. MATERIALS： Forty SAMP8 mice were randomized into four groups： SAMP8 control group, as well as low-, mid-, and high-dose polysaccharide, with 10 mice in each group. Ten senescence accelerated-resistantprone （SAMR 1） mice served as the normal control group. Longyanshen polysaccharides, extracted from the medical plant Longyanshen, were supplied by the Department of Pharmacology, Guangxi Medical University Superoxide dismutase （SOD）, glutathione peroxidase （GSH-Px）, malonaldehyde （MDA）, nitric oxide （NO）, and total protein test kitwere purchased from Nanjing Jiancheng Bioengineering Institute （China）. METHODS： SAMP8 mice were used to establish a dementia animal model. SAMP8 and SAMR1 control mice were administered 30 mL/kg saline. The low-, middle-, and high-dose polysaccharide groups were administered 45, 90, and 180 mg/kg Longyanshen polysaccharides, respectively. Each group was treated by intragastric administration, once daily, for 50 continuous days. MAIN OUTCOME MEASURES： One hour after the last administration, mouse brain tissues were collected, and retro orbital blood sampling was performed. Spectrophotometry was used to measure SOD and GSH-Px activity, as well as MDA and NO concentration in sera and brains of SAMP8 mice. RESULTS： SOD and GSH-Px activity decreased significantly, and MDA and NO concentration increased significantly, in SAMP8 control group brain tissues, compared with the SAMP1 control group （P 〈 0.05）. Compared with the SAMP8 control group, Longyanshen polysaccharide-treated groups exhibited enhanced SOD and GSH-Px activity, as well as decreased MDA and NO concentration, in serum and brain tissue （P 〈 0.05）. Longyanshen polysaccharides exerted a similar effect on SOD, GSH-Px, MDA, and NO concentrations in serum and brain tissues of SAMP8 mice. CONCLUSION： Longyanshen polysaccharides scavenged free radicals effectively, reduced NO concentration and ameliorated NO toxicity, thereby influenced aging and stress, as well as improving memory capacity in the brain.

An enriched environment improves cognitive performance in mice from the senescence-accelerated prone mouse 8 strain Role of upregulated neurotrophic factor expression in the hippocampus

In this study,we examined 3-month-old female mice from the senescence-accelerated prone mouse 8 strain and age-matched homologous normal aging female mice from the senescence accelerated-resistant mouse 1 strain.Mice from each strain were housed in an enriched environment（including a platform,running wheels,tunnel,and some toys）or a standard environment for 3 months.The mice housed in the enriched environment exhibited shorter escape latencies and a greater percentage of time in the target quadrant in the Morris water maze test,and they exhibited reduced errors and longer latencies in step-down avoidance experiments compared with mice housed in the standard environment.Correspondently,brain-derived neurotrophic factor mRNA and protein ex- pression in the hippocampus was significantly higher in mice housed in the enriched environment compared with those housed in the standard environment,and the level of hippocampal brain-derived neurotrophic factor protein was positively correlated with the learning and memory abilities of mice from the senescence-accelerated prone mouse 8 strain.These results suggest that an enriched environment improved cognitive performance in mice form the senescence-accelerated prone mouse 8 strain by increasing brain-derived neurotrophic factor expression in the hippocampus.

Effects of LW-AFC,a new formula derived from Liuwei Dihuang decoction,on intestinal microbiome in senescence-accelerated mouse prone 8 strain,a mouse model of Alzheimer disease

OBJECTIVE To investigate the effects of LW-AFC,a new formula derived fromLiuwei Dihuang decoction,on gut microbiota and the behavior of learning and memory of SAMP8 mice,a mouse model of Alzheimer Disease(AD),and identify the specific intestinal microbiota correlating with cognitive ability.METHODS Morris-water maze test,novel object recognition test and shuttle-box test were conducted to observe the ability of learning and memory.16S rRNA amplicon sequencing(Illumina,San Diego,CA,USA)was employed to investigate gut microbiota.RESULTS The treatment of LW-AFC improved cognitive impairments of SAMP8 mice,including spatial learning and memory ability,active avoidance response,and object recognition memory capability.Our data indicated that there were significantly 8 increased and 12 decreased operational taxonomic units(OTUs)in the gut microbiota of SAMP8 mice compared with senescence accelerated mouse resistant 1(SAMR1) strains,the control of SAMP8 mice.The treatment of LW-AFC altered 22(16 increased and 6 decreased)OTUs in SAMP8 mice and among them,15 OTUs could be reversed by LW-AFC treatment resulting in a microbial composition similar to that of SAMR1 mice.We further showed that there were7(3 negative and 4 positive correlation)OTUs significantly correlated with all the three types of cognitive abilities,at the order level,including Bacteroidales,Clostridiales,Desulfovibrionales,CW040,and two unclassified orders.LW-AFC had influences on bacterial taxa correlated with the abilities of learning and memory in SAMP8 mice and restored them to SAMR1 mice.CONCLUSION The effects of LW-AFC on improving cognitive impairments of SAMP8 mice might be via modulating intestinal microbiome and LW-AFC could be used as a potential anti-AD agent.

Effect of Panax notoginseng saponins on the expression of beta-amyloid protein in the cortex of the parietal lobe and hippocampus, and spatial learning and memory in a mouse model of senile dementia

BACKGROUND： The pharmacological actions of Panax notoginseng saponins （PNS） lie in removing free radicals, anti-inflammation and anti-oxygenation. It can also improve memory and behavior in rat models of Alzheimer＇s disease. OBJECTIVE： Using the Morris water maze, immunohistochemistry, real-time PCR and RT-PCR, this study aimed to measure improvement in spatial learning, memory, expression of amyloid precursor protein （App） and β -amyloid （A β ）, to investigate the mechanism of action of PNS in the treatment of AD in the senescence accelerated mouse-prone 8 （SAMP8） and compare the effects with huperzine A. DESIGN, TIME AND SETTING： A completely randomized grouping design, controlled animal experiment was performed in the Center for Research ＆ Development of New Drugs, Guangxi Traditional Chinese Medical University from July 2005 to April 2007. MATERIALS： Sixty male SAMP8 mice, aged 3 months, purchased from Tianjin Chinese Traditional Medical University of China, were divided into four groups： PNS high-dosage group, PNS low-dosage group, huperzine A group and control group. PNS was provided by Weihe Pharmaceutical Co., Ltd. （batch No.： Z53021485, Yuxi, Yunan Province, China）. Huperzine A was provided by Zhenyuan Pharmaceutical Co., Ltd. （batch No.： 20040801, Zhejiang, China）. METHODS： The high-dosage group and low-dosage group were treated with 93.50 and 23.38 mg/kg PNS respectively per day and the huperzine A group was treated with 0.038 6 mg/kg huperzine A per day, all by intragastric administration, for 8 consecutive weeks. The same volume of double distilled water was given to the control group. MAIN OUTCOME MEASURES： After drug administration, learning and memory abilities were assessed by place navigation and spatial probe tests. The recording indices consisted of escape latency （time-to-platform）, and the percentage of swimming time spent in each quadrant. The number of A β 1-40, A β 1-42 and App immunopositive neurons in the brains of SAMP8 mice was analyzed by immunohistochemistry. The mRNA content ofApp, tau, acetylcholinesterase, and synaptophysin （Syp） was tested by real time PCR and RT-PCR. RESULTS： The PCR results show that PNS can downregulate the expression of the App gene and upregulate the expression of the Syp gene in the parietal cortex and hippocampus of SAMP8 mice. The therapeutic effects of the PNS high-dosage group were greater than those of the PNS low-dosage group and the huperzine A group （P 〈 0.05）. The results of the Morris water maze and immunohistochemistry indicated that PNS can improve the capacity for spatial learning and memory in SAMP8 mice, and reduce the content of A β 1-40, A β 1-42 and expression of App in the brains of SAMP8 mice. The therapeutic effects of the PNS high-dosage group were greater than that of the PNS low-dosage group and the huperzine A group （P 〈 0.05）. CONCLUSION： These results support the hypothesis that PNS plays a therapeutic and protective role on the pathological lesions and learning dysfunction of Alzheimer＇s disease. The therapeutic effects of PNS for Alzheimer＇s disease are possibly achieved through downregulating the expression of the App gene and upregulating the expression of the Syp gene. The therapeutic effects of PNS are dose-dependent and are greater than the effect of huperzine A.

Neuroprotective Effects of Electroacupuncture Preventive Treatment in Senescence-Accelerated Mouse Prone 8 Mice

Objective： To investigate the preventive treatment effects of electroacupuncture（EA） on cognitive changes and brain damage in senescence-accelerated mouse prone 8（SAMP8） mice. Methods： The 5-month-old male SAMP8 and age-matched homologous normal aging mice（SAMR1） were adopted in this study. EA stimulation at Baihui（GV 20） and Yintang（EX-HN 3） was performed every other day for 12 weeks, 4 weeks as a course. Morris water maze test and Nissl-stained with cresyl violet were used for cognitive impairments evaluation and brain morphometric analysis. Amyloid-β（Aβ） expression in hippocampus and parietal cortex was detected by immunohistochemistry, and apoptosis was observed by TUNEL staining. Results： After 3 courses of EA preventive treatment, the escape latencies of 8-month-old SAMP8 mice in EA group were significantly shortened than those of un-pretreated SAMP8 mice. Compared with SAMR1 mice, extensive neuronal changes were visualized in the CA1 area of hippocampus in SAMP8 mice, while these pathological changes and attenuate cell loss in hippocampal CA1 area of SAMP8 mice markedly reduced after EA preventive treatment. Furthermore, Aβ expression in hippocampus and parietal cortex of SAMP8 mice decreased significantly after EA treatment, and neuronal apoptosis decreased as well. Conclusion： EA preventive treatment at GV 20 and EX-HN 3 might improve cognitive deficits and neuropathological changes in SAMP8 mice, which might be, at least in part, due to the effects of reducing brain neuronal damage, decreasing neuronal apoptosis and inhibiting Aβ-containing aggregates.

SAMP8小鼠在中医药抗痴呆中的应用研究进展

快速老化小鼠是一种早期学习记忆障碍模型,因其表现出阿尔茨海默病发病机制的大多数特征,包括抗衰老因子的异常表达、炎症因子的过度升高、淀粉样蛋白沉积、tau蛋白过度磷酸化、线粒体自噬、血脑屏障损伤的中枢机制以及多系统多器官的病理损伤,因而成为阿尔茨海默病(Alzheimer's disease,AD)研究的理想模型而广泛应用。随着AD机制实验研究的不断深入,发现SAMP8小鼠在行为活动、组织病理及生化参数指标上相较于SAMR1发生明显变化,并与人体疾病相类似。基于此,本文对SAMP8小鼠的行为学、组织病理和中医药实验研究进行了系统综述,加深对SAMP8小鼠的认识,了解其生理病理特性,并依据中医药实验研究对其中医证型进行推测,以期对SAMP8小鼠的科学应用提供有益帮助。

lncRNA Gm44981抑制心脏衰老的作用和机制研究

目的分析小鼠心脏衰老过程中长链非编码(lnc)RNA Gm44981的表达水平,探索其抑制心脏衰老的机制。方法选取3月龄年轻和24月龄年老小鼠各5只,提取心肌组织RNA后,采用实时定量聚合酶链式反应(qRT-PCR)检测Gm44981的表达水平。另选取4月龄快速老化小鼠10只,分为对照组和Gm44981过表达组(构建Gm44981过表达快速老化小鼠模型),各5只。采用qRT-PCR检测对照组和Gm44981过表达组小鼠Gm44981和衰老相关分泌表型(SASP)表达水平,β-半乳糖苷酶(SA-β-gal)染色检测SA-β-gal活性,蛋白质免疫印迹试验检测p53和Sirt1衰老相关蛋白表达水平。采用qRT-PCR检测miRNA-34a表达水平。结果Gm44981在年老小鼠的心肌组织中表达水平较年轻小鼠低,差异有统计学意义(P<0.05)。与对照组比较,Gm44981过表达组小鼠Gm44981表达上调,白细胞介素(IL)-1α和IL-6等SASP和SA-β-gal表达下调,p53表达下调,Sirt1表达上调,miRNA-34a表达下调,差异均有统计学意义(P<0.05)。结论lncRNA Gm44981在心脏衰老过程中表达下调,其可能通过作用于miRNA-34a/Sirt1抑制心脏衰老。

全腹辐照后小鼠外周血白细胞、小肠和胸腺组织中衰老相关分泌表型表达的变化

目的:探讨全腹辐照后小鼠小肠、外周血白细胞和胸腺组织中衰老相关分泌表型表达的变化。方法:将24只健康雄性C57BL/6J小鼠随机分为4组(对照组及辐照后3个时间点组),每组6只。对照组不接受辐照,其余3组小鼠接受16 Gy 60 Coγ射线全腹照射,分别在辐照后第2 h、第3天和第7天取外周血、小肠和远端胸腺组织,HE染色观察组织损伤情况,γ-H2AX免疫荧光染色检测DNA损伤程度,RT-qPCR法检测IL-1β、TNF-α、Cxcl2及p21 mRNA的表达,免疫组化法检测胸腺组织中TNF-α的表达。结果:与正常对照组比较,3个辐照组小鼠小肠组织有明显损伤,胸腺组织有一定程度组织结构异常;全腹辐照后第2 h组小肠组织和外周血白细胞中γ-H2AX阳性信号数增加,辐照后第3天和第7天组小鼠胸腺组织中γ-H2AX阳性信号数增加(P均<0.001)。辐照后第3天和第7天组外周血白细胞、小肠和胸腺组织中p21、IL-1β、TNF-α、Cxcl2 mRNA表达水平均升高(P均<0.05),胸腺组织中TNF-α蛋白表达增加(P<0.001)。结论:全腹辐照可导致小鼠远端胸腺组织发生DNA损伤和炎症反应。

快速老化SAMP6小鼠骨代谢及其分子机制研究进展

老年性骨质疏松(senile osteoporosis, SOP)是一种易发骨折的全身性骨病,发病过程复杂,机制研究不足。目前,快速老化小鼠P6品系(senescence accelerated mouse prone 6,SAMP6)是用于研究SOP发病机制和防治SOP的理想模型。该模型表现出骨脆性增加、骨微观结构退化、骨基质流失、骨内细胞代谢异常与功能紊乱等特征,从宏观到微观均能复制SOP发生和发展的过程。

快速老化模型小鼠海马蛋白质组学初步研究

应用双向凝胶电泳结合质谱鉴定,分析比较6月龄和12月龄快速老化模型小鼠(Senescence-accele-rated mouse,SAM)的快速老化亚系SAM-prone/8(SAMP8)及抗快速老化亚系SAM-resistance/1(SAMR1)海马蛋白表达的差异,从蛋白质水平初步探讨与老化相关的学习记忆功能障碍的发生机制.结果表明,与同龄SAMR1比较,6月龄SAMP8海马中有15个蛋白点表达显著上调,5个蛋白点表达显著下调;12月龄SAMP8海马中有12个蛋白点表达显著上调,2个蛋白点表达显著下调,2个蛋白点只在SAMP8中有表达.应用质谱分析结合数据库检索,共鉴定了22种蛋白质.6月龄和12月龄SAMP8与SAMR1海马中表达有明显变化的蛋白按功能可分为如下4类:(1)能量代谢相关蛋白;(2)线粒体功能相关蛋白;(3)信号转导相关蛋白;(4)其它蛋白.研究结果表明,SAMP8和SAMR1海马蛋白表达存在明显差异,其中一些蛋白与SAMP8随龄出现的学习记忆功能减退相关,并可能为研究或发现促智药物作用的新蛋白靶标提供线索.

远志总苷对快速老化模型(SAM-P/8)小鼠学习记忆能力的作用及其机理研究

目的探讨远志总苷对快速老化模型小鼠学习记忆能力的作用及其机制。方法以SAM-P/8小鼠为对象,给予远志总苷,连续灌胃30d,采用水迷宫方法逐日测定小鼠的学习记忆能力,用化学比色法测定脑组织总蛋白含量、总抗氧化能力和乙酰胆碱酯酶活性,用放免法测定血清中IL-2含量。结果远志总苷能明显提高SAM-P/8小鼠的学习记忆能力,缩短到达目的地的时间;显著提高脑组织总蛋白含量、总抗氧化能力、降低乙酰胆碱酯酶活性及血清中IL-2含量。结论远志总苷可提高SAM-P/8小鼠的学习记忆能力,其作用机理可能与降低脑组织氧化损伤有关。

针刺肾俞穴对SAMP6小鼠股骨生物力学性能的影响

目的探讨针刺肾俞穴治疗骨质疏松的机制。方法采用放免法测定快速老化小鼠P6(senes- cence accelerated mouse prone 6,SAMP6)及其正常对照抗快速老化小鼠R1(senescence accelerated mouse re- sistant 1,SAMR1)血清睾酮(T)、骨钙素(BGP)水平;三点弯曲试验法测定其股骨生物力学性能,观察针刺对SAMP6小鼠股骨力学性能、骨矿含量等的影响。结果与SAMR1[T(20.91±3.41)nmol/L,BGP(6.71±2.07)μg/L]比较,SAMP6小鼠血清T[(11.09±1.48)nmol/,L]水平下降(P<0.01),BGP[(12.29±2.29)μg/L]水平上升(P<0.01);股骨弯曲强度下降,脆性增加。针刺肾俞穴后,上述指标均有不同程度改善,并趋于正常,血清T(15.05±2.63)nmol/L、BGP(8.88±1.85)μg/L,与SAMP6组比较,差异有统计学意义(P<0.05,P<0.01)。结论针刺肾俞穴可有效阻止SAMP6小鼠骨丢失,增强其骨强度。其治疗作用部分是通过促进性激素分泌,改善骨代谢,降低骨转换率,增加骨量等达到的。

自愿运动对快速老化小鼠学习记忆能力和海马生长相关蛋白43的影响

目的观察自愿运动对快速老化小鼠(senescence-accelerated mouse prone 8,SAMP8)学习记忆能力和海马生长相关蛋白43(growth-associated protein-43,GAP43)表达的影响,探讨运动提高认知能力延缓衰老的机制。方法 60只3个月龄雌性SAMP8小鼠随机平均分为跑笼环境组(RCE组)和标准环境组(SE组)。饲养3个月后,用Morris水迷宫测试小鼠的寻找平台潜伏期及搜索策略。行为学测试后,各组分别取10只小鼠的鼠脑用RT-PCR法检测海马GAP43mRNA的表达;取10只小鼠的鼠脑用免疫印迹实验检测海马GAP43蛋白的表达;剩余10只取鼠脑用免疫组织化学实验观察海马GAP43免疫反应产物的表达。结果 Morris水迷宫实验表明RCE组小鼠寻找平台潜伏期较SE组缩短(P<0.01,P<0.05),在第Ⅰ象限游泳时间比SE组延长(P<0.01),在第Ⅳ象限游泳时间比SE组缩短(P<0.05)。RCE组与SE组比较,海马GAP43表达增加(P<0.01)。结论自愿运动能提高SAMP8小鼠学习记忆能力,其机制可能与运动能促进海马GAP43表达有关。

六味地黄多糖体外对正常及衰老小鼠脾细胞免疫功能的影响

目的探讨六味地黄多糖免疫药理活性的物质基础。方法运用现代药理学与植物化学紧密配合的方法，从六味地黄汤中逐步分离获得了六味地黄多糖ＣＡ４３Ｂ和Ｐ３。应用［３Ｈ］ＴｄＲ参入法和溶血空斑实验观察了其体外对小鼠脾细胞免疫功能的作用。结果ＣＡ４３Ｂ、Ｐ３体外单独使用对正常及快速老化模型ＳＡＭＰ８和ＳＡＭＲ１小鼠脾细胞增殖反应有明显的促进作用，但不能增强有丝分裂原ＣｏｎＡ诱导的脾细胞增殖反应，大剂量时有一定的抑制作用。ＣＡ４３Ｂ对绵羊红细胞（ＳＲＢＣ）体外诱导的正常小鼠脾抗体形成细胞生成反应亦有明显的促进作用，使抗体形成细胞（ＰＦＣ）的数目明显增加。结论ＣＡ４３Ｂ和Ｐ３可能为具有免疫调节作用的活性多糖。

黄连解毒汤对快速老化模型小鼠海马蛋白表达的影响

目的:研究黄连解毒汤(HLJDT)对快速老化模型小鼠(senescence accelerated mouse,SAM)的快速老化亚系SAM-prone/8(SAMP8)海马蛋白表达的影响,以期从分子水平较深入地阐明HLJDT治疗阿尔茨海默病(AD)的机制。方法:将12月龄SAM的快速老化亚系SAMP8和抗快速老化亚系SAM-resistance/1(SAMR1)分为SAMR1对照组、SAMP8模型组和HLJDT给药组,应用双向凝胶电泳结合质谱鉴定,观察HLJDT对SAM海马组织蛋白表达的影响。结果:与SAMR1相比,SAMP8海马中有29个蛋白点的表达发生显著变化;给予HLJDT后有38个蛋白点的表达发生显著变化。选取部分HLJDT的作用蛋白点进行质谱分析结合数据库检索,共鉴定出12个蛋白,这些蛋白涉及到能量代谢、转录调控、细胞骨架、氨基酸代谢等功能。其中有4个蛋白是SAMP8与SAMR1海马蛋白比较存在显著差异的蛋白,给予HLJDT后其蛋白表达得到了明显改善。结论:HLJDT通过调节SAMP8脑中与能量代谢、信号转导、细胞骨架及氨基酸代谢等相关蛋白的表达,从多途径对SAMP8的老化起到了改善作用。

抗氧化剂TA9901抑制加速老化鼠脑淀粉样颗粒的沉积

目的 观察抗氧化剂TA990 1对加速老化鼠P 8(SAM P 8)脑中淀粉样颗粒 (MSG)沉积的影响 ,为临床治疗阿尔采默病 (AD)提供科学依据。 方法 2 5月龄雄性SAM P 8小鼠随机分为对照组、TA1组、TA2组和VE组 ,分别给予正常饮食、0 0 5 %TA990 1、0 5 %TA990 1和特制VitaminE(VE)饲料 (5 0 0mgVE kg)喂养 3 5个月。用Go mori六胺银法显示淀粉样颗粒 ,对海马CA1区的银染颗粒 (MSG)的体视学参数和分布进行图像分析。 结果 MSG为圆形和卵圆形 ,主要分布于海马、皮质深层和小脑 ;海马内MSG主要成群分布于各层。各组海马CA1区MSG颗粒数比较 ,差异均无显著性 (P >0 0 5 ) ,但TA1组、TA2组和VE组的MSG颗粒直径和面积均较对照组明显减小 (P <0 0 5 ) ,以TA2和VE组更为显著 (P <0 0 1) ;各实验组MSG的平均灰度均较对照组降低 (P <0 0 1) ;对照、TA1、TA2和VE组的低密度颗粒区分别占 12 0 5 %、36 5 2 %、4 7 91%和 4 4 6 5 % ,实验组在低密度区的颗粒数明显增多。 结论 TA990 1减少了SAM P 8脑中淀粉样颗粒的大小和密度 ,显示TA990

三七总皂苷对快速老化模型小鼠SAMP8脑内APP基因转录的影响

目的:研究三七总皂苷(PNS)对快速老化模型小鼠(SAMP8)学习记忆能力及脑内淀粉样前体蛋白(APP)基因转录水平的影响。方法:将SAMP8随机分为PNS高剂量组、PNS低剂量组、石杉碱甲(阳性对照组)组、模型组,各给药组分别按设定剂量灌胃给药,模型组给予等体积双蒸水灌服,连续8 w后应用Morris水迷宫、实时逆转录聚合酶链式反应(RT-PCR)的方法,检测PNS高、低剂量组SAMP8学习记忆和脑内APP mRNA含量的影响。结果:PNS能改善SAMP8的学习记忆能力(P<0.05或P<0.01),PNS高剂量还能显著降低其脑内APP mRNA含量(P<0.05)。结论:PNS能显著改善SAMP8的学习记忆能力,其作用途径可能与在转录水平下调APP基因的表达有关。

栎金钱菌活性提取物抗衰老研究

用栎金钱菌活性提取物灌胃衰老模型小鼠,观察其对小鼠血清SOD活性、肝组织MDA和脂褐素的含量、脾指数、胸腺指数和肾指数的影响。结果表明,栎金钱菌活性提取物能使雄性小鼠血清SOD活性提高40.16%,肝MDA含量减少47.12%,肝脂褐素含量减少89.48%,脾指数增加35.13%,胸腺指数增加48.92%,肾指数增加11.26%,表明栎金钱菌活性提取物具有良好的抗衰老作用。栎金钱菌活性提取物800mg/kg·d的剂量具有最好的抗衰老效果,且具有性别的差异,对雄性小鼠的抗衰老作用略优于对雌性小鼠的。

快速老化小鼠SAMP8研究进展

快速老化小鼠SAMP8(senescence-accelerated mouseprone/8)是一个从普通的遗传群AKR/J系小鼠中通过表型选择培育出的快速老化小鼠,表现为早期增龄性学习记忆缺陷,同时伴有Aβ淀粉样蛋白沉积,是目前公认的有效的研究阿尔采末病(Alzheimer’s disease,AD)动物模型。同属SAMR1表现为抗快速老化,具有正常的老化特性,常用作正常对照。目前SAMP8已被广泛应用于研究快速学习记忆缺陷的发病机制,以及评价抗衰老及改善学习记忆功能的药物等。

快速老化小鼠——研究衰老及衰老相关疾病的动物模型

快速老化小鼠 (Senescenceacceleratedmouse,SAM)分为快速老化亚系 (Senescenceacceleratedmouse/ prone,SAMP)及抗快速老化亚系 (Senescenceacceleratedmouse/re sistance ,SAMR)。由日本京都大学首次培育成功 ,目前共有12个亚系 ,不同亚系具有不同的病理表现型 ,其中许多具有与人类衰老相似的病理学特征。人类许多老年性疾病如肺泡扩张、骨质疏松、骨关节疾病、学习记忆功能障碍、情感紊乱 (抑郁 )、白内障、听觉障碍、脑萎缩、免疫缺陷等在SAMP不同亚系上均有不同程度的体现 ,而SAMR亚系的各项生理指标及生存期限与正常动物相似。因此 ,SAM (SAMP、SAMR)为探讨衰老及衰老相关疾病的发生机制 ,评价药效及其作用机制提供了良好的动物模型。