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1.
脑是有机体衰老过程中最突出的器官,也是人和动物老年性功能障碍的主要病灶之一。本文阐述了衰老脑的特征、衰老动物在机能方面所表现的机能障碍、脑衰老机理的研究概况和改变脑衰老过程的一些措施。指出,目前用于脑衰老研究的主要是啮齿类鼠、兔等动物模型,其研究结果很难肯定完全符合于灵长类或其它脊椎动物。因此,动物模型的建立和评价已经成为脑衰老研究的当务之急。  相似文献   

2.
脑衰老机制与脑疾病的关系   总被引:3,自引:0,他引:3  
衰老是人类生命过程的必然规律,是不可抗拒的自然现象.神经系统是重要的机能调节系统,也是受衰老影响最大的系统之一,衰老的脑组织会产生一些特征性的改变,了解这些改变及其分子机制对衰老的研究具有重要意义.本文就近年来脑与衰老的研究进行综述,以进一步探讨脑衰老和脑衰老相关疾病的机制.  相似文献   

3.
中老年磁疗     
人的衰老是整体的,由于人们的遗传因素及日常生活工作中所处的地位、环境、生活习惯不同,出现衰老的年岁也不同,局部表现也不同。即使是一个人,衰老的脏腑器官也不尽相同,有的脑子先衰老,有的心、有的肺部先衰老。伴随这些衰老性变化,常有不同的退行性病变。下面介绍中老年常见病磁疗。脑部病症的磁疗年逾40岁后,脑细胞数目逐渐减少,脑重量也随之减轻,60岁后减少更显著。其原因是脑组织代谢不良和供血减少。脑动脉硬化和供血不足,对老年人尤为常见,它是全身动脉硬化的局部表现,随年龄逐渐加重。并伴有高血压病,有的导致脑…  相似文献   

4.
细胞衰老是一个体内平衡的生物过程,在推动机体衰老过程中起着关键作用。衰老细胞在神经系统中随着衰老和神经退行性疾病而积累,并且可能使人易患神经退行性疾病或加重其病程。帕金森病(Parkinson's disease,PD)是一种与年龄相关的神经退行性疾病。运动可通过提高衰老过程中脑细胞自噬水平,增强神经免疫信号分子以及脑内脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)的表达有效预防或延缓脑细胞衰老甚至清除脑衰老细胞,维持脑健康。大量流行病学调查结果以及临床和基础研究证实,不同形式的运动锻炼/身体活动均可改善PD患者或者PD模型动物的症状或改善症状的发展。本文以脑衰老胶质细胞为切入点,充分阐明脑衰老胶质细胞在PD中的作用以及运动干预对PD脑衰老胶质细胞的影响,以便有效和安全地利用脑衰老胶质细胞作为潜在的治疗靶点,以期为运动干预减缓(和)或改善PD运动功能障碍的神经生物学机制研究提供新的思路,为探寻PD的非药物防治或辅助疗法提供理论基础。  相似文献   

5.
概述了脑与衰老在神经分子生物学方面的研究进展 ,包括 :细胞衰老分子机制的主要进展 ,衰老脑在基因及其表达水平的研究进展 ;阿尔茨海默病 (AlzheimerDisease ,AD)相关基因研究进展 ,帕金森病 (porkinsondisease ,PD)相关基因研究进展[7] 。这些研究成果对脑与衰老的关系、对脑在基因及其表达水平上衰老机制认识的加深乃至对衰老脑的基因治疗均具有理论意义和应用价值。  相似文献   

6.
胎脑提取液对衰老小鼠肝细胞酶活性影响的实验研究   总被引:2,自引:0,他引:2  
目的:观察胎脑提取液对衰老小鼠肝细胞琥珀酸脱氢酶(SDH)和酸性磷酸酶(ACP)活性的影响,探讨胎脑提取液的抗衰老作用。方法:选用健康昆明种小白鼠30只,随机分为3组;采用D-半乳糖制备亚急性衰老模型;酶组织化学染色观察各组小鼠肝细胞SDH和ACP的活性。结果:衰老模型组与正常对照组相比,小鼠肝细胞SDH活性明显降低,ACP活性明显升高;给药组与衰老模型组相比,小鼠肝细胞SDH活性明显升高,ACP活性明显降低。结论:胎脑提取液可以延缓肝细胞的衰老进程,具有一定的抗衰老作用。  相似文献   

7.
胎脑提取液对衰老小鼠海马神经元酶活性影响的实验研究   总被引:2,自引:0,他引:2  
目的 观察胎脑提取液对衰老小鼠海马神经元酸性磷酸酶(ACP)和琥珀酸脱氢酶(SDH)活性的影响,探讨胎脑提取液的抗衰老作用。方法 选用健康昆明种小白鼠30只,随机分为3组;采用D-半乳糖制备亚急性衰老模型;酶组织化学方法结合显微图像分析。观察各组小鼠海马神经元ACP和SDH的活性。结果 衰老模型组与正常对照组相比,小鼠海马神经元ACP活性明显升高,SDH活性明显降低;给药组与衰老模型组相比,小鼠海马神经元ACP活性明显降低。SDH活性明显升高。结论 胎脑提取液可以延缓海马神经元的衰老进程,具有一定的抗衰老作用。  相似文献   

8.
综述:脑衰老与阿尔茨海默病症状出现前阶段   总被引:1,自引:0,他引:1  
脑衰老可分为生理性增龄变化与病理性变化,后者与阿尔茨海默病(Alzheimer's disease,AD)等神经退行性疾病的发生有关.生理性脑衰老与AD在发病早期具有相似的表现形式、病变特征、生化改变和发病机制.其共同的分子机制是异常蛋白质蓄积,提示两者有着相似的病理学基础,脑衰老可能是AD等神经退行性改变的最初级阶段,病理性脑衰老因素可能促进AD等神经退行性疾病的发生发展.临床前期AD(preclinical AD,PCAD)患者的脑、血液和脑脊液中可以检测到AD特定的生物标记物,但AD的临床症状并没有出现,因此也被称为“症状出现前AD(presymptomatic AD)”.PCAD和对照组比较,氧化应激指标和高度不溶性Aβ42并没有显著性升高,寻找早期PCAD发病过程中新的可用于临床早期诊断的生物标记物、药物靶点将成为我们的关注重点.  相似文献   

9.
商晓康  张思萌  倪军军 《遗传》2023,(3):212-220
组织蛋白酶B (cathepsin B,CatB)是一种定位于溶酶体的半胱氨酸蛋白酶,最初被认为在溶酶体内发挥非选择性地降解吞噬或者自噬蛋白的功能。然而最新研究发现,CatB也可以选择性地降解或特异性地活化目标蛋白,从而参与调控生理病理反应。在衰老及相关的神经退行性疾病的大脑中,CatB的表达、酶活性及细胞定位都发生了显著变化,因此CatB在衰老和神经退行性疾病中的病理学功能备受关注。本文对CatB参与脑衰老及阿尔兹海默症进程的相关研究进行了系统梳理,并讨论了目前有关CatB的神经病理学研究中存在的问题,以期为全面认识脑衰老及阿尔兹海默症的病理机制奠定基础。  相似文献   

10.
花粉制剂对脑衰老动物各脑区的SOD和NO水平的影响   总被引:2,自引:0,他引:2  
采用 D-半乳糖建立脑衰老动物模型 ,观察服用花粉制剂前后对脑衰老模型动物不同脑区组织中超氧化物歧化酶 ( SOD)活性、一氧化氮 ( NO)水平的影响。结果表明花粉制剂能明显升高脑衰老动物某些脑区 SOD活性和降低脑衰老动物某些脑区 NO水平。研究结果提示花粉制剂具有延缓衰老和增强记忆力等作用 ,其机制可能与其促进自由基的清除及减少 NO释放有关。  相似文献   

11.
衰老大鼠的某些脑区组织中游离氨基酸水平的改变   总被引:2,自引:1,他引:1  
使用D 半乳糖建立衰老大鼠模型组与同龄、同饲的正常对照组大鼠的某些脑区游离氨基酸 (FAA)水平的比较发现 :( 1 )衰老模型组的海马、纹状体以及皮层等脑区中谷氨酸 (Glu)、天门冬氨酸 (Asp)水平明显降低 ;( 2 )γ 氨基丁酸 (GABA)水平在衰老模型组大鼠的海马 ,纹状体以及小脑等脑区中明显升高 ;( 3)衰老模型组的皮层、小脑、海马、纹状体等脑区的牛磺酸 (Tau)水平明显下降。以此探讨动物衰老与脑区游离氨基酸水平的关系  相似文献   

12.
目的:观察Deoxygedunin对D-半乳糖联合AlCl3诱导的阿尔茨海默病模型大鼠Aβ沉积、学习记忆和氧化应激的影响及其可能机制。方法:健康成年雄性SD大鼠随机分为3组(n=12):对照组(Control)、模型组(AD)和干预组(AD+Deo)。Morris水迷宫实验检测大鼠学习记忆和认知功能;采用酶联免疫吸附法(ELISA)检测大鼠海马组织匀浆中谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)和丙二醛(MDA)含量;免疫组织化学检测大鼠大脑皮层tau蛋白表达情况;Western blot实验用于检测TrkB信号通路上ERK1、AKT和TrkB蛋白的表达。结果:水迷宫结果显示,与对照组相比,D-半乳糖联合AlCl3诱导的大鼠逃避潜伏期显著增加(P<0.05)。Deoxygedunin可逆转模型组逃避潜伏期的增加(P<0.05)。在去除平台的第7日,与对照组和干预组相比,模型组大鼠表现出逃避潜伏期增加(P<0.01),穿越平台次数较少(P<0.05);免疫组织化学和ELISA实验结果显示,与对照组相比,模型组Aβ、tau蛋白表达显著增加(P<0.01),SOD、GSH-Px活性显著降低,MDA含量明显升高。与模型组相比,Deoxygedunin可逆转模型组Aβ、tau蛋白表达的增多(P<0.01),SOD、GSH-Px活性显著降低(P<0.05),MDA含量明显升高(P<0.05);Western blot结果显示,Deoxygedunin干预可逆转模型组海马TrkB、AKT和ERK1的磷酸化水平的降低。结论:Deoxygedunin可通过激活TrkB信号转导通路显著逆转Aβ沉积,氧化应激和认知缺陷,提示Deoxygedunin可能作为减轻D-半乳糖联合AlCl3诱导AD样病理功能障碍潜在的治疗备选药物。  相似文献   

13.
Metabotrophic glutamate receptors (mGluRs) modulate cellular activities involved in the processes of differentiation and degeneration. In this study, we have analysed the expression pattern of group-I metabotropic glutamate receptor (mGlu-5) in cerebral cortex, corpus striatum, brainstem and hippocampus of streptozotocin induced and insulin treated diabetic rats (D+I) as a function of age. Also, the functional role of glutamate receptors in intra cellular calcium release from the pancreatic islets was studied in vitro. The gene expression studies showed that mGlu-5 mRNA in the cerebral cortex increased siginficantly in 7 weeks old diabetic rats whereas decreased expression was observed in brainstem, corpus striatum and hippocampus when compared to control. 90 weeks old diabetic rats showed decreased expression in cerebral cortex, corpus striatum and hippocampus whereas in brainstem the expression increased significantly compared to their respective controls. In 7 weeks old D+I group, mGlu-5 mRNA expression was significantly decreased in cerebral cortex and corpus striatum whereas the expression increased significantly in brainstem and hippocampus. 90 weeks old D+I group showed an increased expression in cerebral cortex, while it was decreased significantly in corpus striatum, brainstem and hippocampus compared to their respective controls. In vitro studies showed that glutamate at lower concentration (10-7 M) stimulated calcium release from the pancreatic islets. Our results suggest that mGlu-5 receptors have differential expression in brain regions of diabetes and D+I groups as a function of age. This will have clinical significance in management of degeneration in brain function and memory enhancement through glutamate receptors. Also, the regulatory role of glutamate receptors in calcium release has immense therapeutic application in insulin secretion and function.  相似文献   

14.
目的: 研究虾青素复合有氧运动对D-半乳糖诱导大鼠肾脏衰老的干预作用及其机制。方法: 60只3月龄SPF级SD大鼠采用两因素两水平2×2析因设计随机分为空白对照组(C组)、急性衰老组(S组)、虾青素+急性衰老组(AS组)、有氧运动+急性衰老组(ES组)、虾青素+有氧运动+急性衰老组(AES组),每组12只。大鼠腹腔注射100 mg/(kg·d) D-半乳糖复制经典急性衰老模型,并分别以20 mg/(kg·d) 虾青素和/或强度为60%最大摄氧量的有氧运动进行干预,实验周期6周。末次训练12 h后取肾脏,光镜/电镜观察肾脏组织形态/超微结构,酶联免疫吸附法检测肾脏组织超氧化物歧化酶(SOD)、γ-谷氨酸半胱氨酸合酶(γ-GCS)活性及丙二醛(MDA)含量,荧光比色法检测肾脏组织脂褐质(LDF)含量,免疫组化法检测肾脏组织核因子E2相关因子2(Nrf2)通路蛋白质表达水平。结果: 与AS、ES组比较:AES组肾脏组织形态/超微结构改善更为显著;LDF含量均显著降低(P<0.01);SOD活性均显著升高(P<0.01);γ-GCS活性显著高于AS组,而与ES组无显著性差异(P>0.05);MDA含量组间无显著性差异(P>0.05);Nrf2、磷酸化核因子E2相关因子2(p-Nrf2)蛋白质表达均显著升高(P<0.05,P<0.01);抗氧化酶血红素氧合酶1(HO-1)蛋白质表达显著高于ES组(P<0.05),而与AS组无显著性差异(P<0.05)。结论: 虾青素复合有氧运动可以延缓肾脏衰老,其作用机制可能为调控Nrf2信号通路相关蛋白质表达及下游Ⅱ相解毒酶和抗氧化酶活性,改善D-半乳糖致衰大鼠肾脏氧化应激。  相似文献   

15.
Gao YQ  Gao H  Zhou ZY  Lu SD  Sun FY 《生理学报》2004,56(2):153-157
实验在大鼠大脑中动脉阻塞性脑缺血(middle cerebral arterv occlusion,MCAO)模型上采用Western Blot方法检测脑缺血再灌注不同时程(6h、12h、1d、3d)脑组织中瞬时受体电位通道蛋白4(transient receptor potential channel4,TRPC4)的表达情况,并与正常对照组相比,结果显示,12 h、1 d、3 d组纹状体、海马区域TRPC4含量明显高于正常组(P<0.05)。采用免疫组织化学定位检测,显示TRPC4主要表达在神经元细胞膜上;免疫组化阳性细胞统计分析显示,在不同时程缺血组中纹状体、海马区域TRPC4的表达与正常组相比有所增加,其中纹状体、海马区缺血再灌注1 d、3 d组缺血同侧1RPC4阳性细胞升高显著(P<0.05)。脑缺血再灌注损伤后TRPC4相对含量增加,提示TRPC4可能参与脑缺血引起的急性和迟发性神经元损伤。  相似文献   

16.
Hypertension, aging and a range of neurodegenerative diseases are associated with increased oxidative damage. The present study examined whether superoxide (O2•-) levels in brain are increased during aging in female rats, and the role of superoxide dismutase (SOD) and oestrogen in regulating O2•- levels.

Young adult (3 month) and old (11 month) female spontaneously hypertensive stroke prone rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY) were studied. O2•- levels were measured in brain homogenates by lucigenin chemiluminescence and SOD expression by Western blotting. Ageing significantly increased brain O2•- levels in WKY (cortex +216%, hippocampus +320%, striatum +225%) and to a greater extent in SHRSP (cortex +540%, hippocampus +580%, striatum +533%). Older SHRSP showed a decline in cortical Cu/Zn SOD expression compared to young adult SHRSP. Oestrogen did not attenuate O2•- levels.

The results show a significant age-dependent increase in brain O2•- levels which is exaggerated in SHRSP. The excess cortical O2•- levels in the SHRSP may be associated with a down-regulation of Cu/Zn SOD but are not related to a decrease in oestrogen.  相似文献   

17.
The present study was undertaken in order to investigate the muscarinic (M(1)), dopaminergic (D(1) and D(2)) and serotonergic (5-HT(2)) receptors densities in hippocampus and striatum of Wistar rats after status epilepticus (SE) induced by pilocarpine. The control group was treated with 0.9% saline. An other group of rats received pilocarpine (400 mg/kg, s.c.) and both groups were sacrificed 1 h after treatment. The results have shown that pilocarpine administration and resulting SE produced a downregulation of M(1) receptor in hippocampus (41%) and striatum (51%) and an increase in the dissociation constant (K(d)) values in striatum (42%) alone. In both areas the 5-HT(2) receptor density remained unaltered, but a reduction (50%) and an increase (15%) in the K(d) values were detected in striatum and hippocampus, respectively. D(1) and D(2) receptor densities in hippocampus and striatum remained unaltered meanwhile K(d) values for D(1) receptor declined significantly, 33% in hippocampus and 26% in striatum. Similarly, K(d) values for D(2) decreased 55% in hippocampus and 52% in striatum. From the preceding results, it is clear that there is a possible relation between alterations in muscarinic receptor density and others systems studied as well as they suggest that changes in dissociation constant can be responsible for the establishment of pilocarpine-induced SE by altering the affinity of neurotransmitters such as acetylcholine, dopamine and serotonine.  相似文献   

18.
Rats received a solution of sodium barbitone as their only drinking fluid for 33 and 42–44 weeks. In three groups (A3, A12 and A30) the barbitone solution was withheld and replaced by water 3, 12 and 30 days respectively before death. Two other groups consisted of animals drinking barbitone until death (B) and untreated controls (C). Abstinence convulsions were recorded by jiggle cages. Thirty nmol of tritium-labelled choline ([3H]Ch) were injected i.v. and the rats were killed by decapitation 1 min later. A significantly higher content of tritium-labelled acetylcholine ([3H]ACh) was found in the cerebellum + medulla oblongata + midbrain of rats receiving barbitone until death (group B) (+22%) and abstinent for 3 days (+54%) (group A3) compared with group C. The [3H]ACh content was also significantly increased in the hippocampus + cortex of rats abstinent for 3 days (+23%). In the striatum no significant effect on [3H]ACh content was found in any of the groups. The ratio [3H]ACh/[3H]Ch was significantly increased in the cerebellum + medulla oblongata + midbrain of rats in group B and A3 and in the hippocampus + cortex in group A3. These results might indicate an increased turnover of ACh. The effect of long-term barbitone treatment on the enzyme activities of brain choline acetyltransferase and acetylcholinesterase was also studied but no significant effect was found.  相似文献   

19.
目的:探讨二甲双胍(Met)对D-半乳糖(D-gal)诱导雄性中年小鼠衰老的干预作用。方法:50只ICR 9月龄雄性小鼠,在SPF级实验环境饲养,自由摄食与饮水。随机分5组:对照组,模型组,二甲双胍低、中、高剂量(Met 50 mg/kg,Met 100 mg/kg,Met 200 mg/kg)组,每组10只。Met组和模型组小鼠每日颈背部皮下注射D-gal 100 mg/ kg,同时分别给予Met(50、100、200 mg/kg)或等体积NS灌胃。对照组注射和灌胃等体积NS。连续8周给药。检测小鼠一般状态,体重,空腹血糖,血清和肝脏超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量水平;水迷宫实验检测学习记忆能力;HE染色观察小鼠海马组织结构。结果:每日Met 200 mg/kg干预,能减少模型小鼠的体重。Met干预对模型鼠正常空腹血糖无影响。每日Met 50、100、200 mg/kg剂量干预,与模型组相比,均能显著提升模型小鼠血清和肝组织的SOD活性(P<0.05)、降低血清MDA含量(P<0.05),改善学习记忆能力测试的大部分指标(P<0.05),HE染色显示海马齿状回核固缩、深染的神经元明显减少。Met干预在大部分指标上呈剂量-效应依赖关系。结论:每日Met 50~200 mg/kg长期处理,以Met 200 mg/kg为显著,能延缓D-gal 诱导的雄性中年衰老模型小鼠的衰老进程,机制可能与降低小鼠体重与增强机体抗氧化水平有关。  相似文献   

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