枸杞对D-半乳糖致衰老小鼠学习记忆影响

目的观察枸杞对D-半乳糖所致衰老小鼠学习记忆的影响。方法建立D-半乳糖致衰老小鼠模型，跳台实验检测其学习记忆能力，同时测定其大脑乙酰胆碱酯酶（AchE）活性，用黄嘌呤氧化酶法测定大脑超氧化物歧化酶（soD）活性，硫代巴比妥法测定大脑丙二醛（MDA）含量，观察小鼠服用枸杞汁后上述指标变化。结果与D一半乳糖模型组比较，各实验组均可提高小鼠的学习记忆能力（P〈0．05或P〈0．01），显著增加D-半乳糖所致衰老小鼠大脑SOD活性、降低MDA含量（P〈0．05或P〈0．01），可显著升高大脑AchE活性（P〈0．05，或P〈0．01）。结论枸杞能改善D-半乳糖所致衰老小鼠的学习记忆功能，其机制可能与枸杞的抗氧化自由基作用有关。     

新疆油菜花粉对D-半乳糖致衰老小鼠抗氧化作用的实验研究

[目的]观察新疆油菜花粉对D-半乳糖所致衰老小鼠的抗氧化作用.[方法]用D-半乳糖复制亚急性衰老小鼠模型.实验分空白对照组、模型对照组、花粉组(2g.kg-1. d-1和4g.kg<-1.d-1)和维生素E组(100mg.kg-1. d-1),实验6周后处死动物,测定血清、肝脏及脑组织中的丙二醛(MDA)含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性.[结果]花粉可显著降低衰老小鼠血清、肝脏及脑组织中的MDA含量,提高SOD、 GSH-Px活性.[结论]花粉有一定的抗衰老作用.     

不同茶叶对D-半乳糖衰老小鼠抗氧化作用比较

目的 比较4种不同发酵类型茶叶对D-半乳糖衰老小鼠的抗氧化作用。方法 将小鼠随机分为7组(对照组、模型组、绿茶组、乌龙茶组、红茶组、黑茶组和阳性对照组),除对照组外,其余6组皮下注射D-半乳糖建立氧化损伤动物模型,在造模同时各茶叶组和阳性对照组分别灌胃茶叶水(2 g/kg)和维生素C(10 mg/kg),30 d后处死小鼠测定脏器指数,血清、肝脏和脑组织SOD、CAT活力和T-AOC。结果 绿茶能提高D-半乳糖模型小鼠肝脏、脑组织、脾脏和胸腺脏器指数,差异有统计学意义(P<0.05);绿茶组血清SOD、CAT活力和T-AOC分别为(139.18±8.19)、(6.03±0.56)和(17.67±0.71)U/mL,与模型组比较,明显升高,差异有统计学意义(P<0.01);绿茶、红茶和黑茶对肝脏和脑组织SOD、CAT活力和T-AOC均有提高作用(P<0.05),且绿茶效果强于红茶和黑茶。结论 不同发酵类型茶叶对D-半乳糖衰老小鼠均具有抗氧化作用,其中绿茶在4种发酵类型茶叶中抗氧化能力最强。     

海兔素对D-半乳糖诱导衰老小鼠抗氧化作用

目的 通过对D-半乳糖导的衰老小鼠补充不同剂量海兔素,观察其对DNA损伤和机体抗氧化能力影响.方法 以D-半乳糖连续颈背皮下注射制作亚急性衰老小鼠模型,并测定血淋巴细胞DNA损伤状况、血浆中O6-甲基鸟嘌呤(O6-MeG)含量以及血清中抗氧化酶活力.结果 海兔素各剂量组的血淋巴细胞自发性损伤程度差异无统计意义.经H2O2处理后,海兔素中、高剂量组及维生素E对照组血淋巴细胞DNA损伤程度及血浆中O6-MeG含量均低于模型组(P<0.05).海兔素低、中、高剂量组及维生素E对照组血清中丙二醛(MDA)含量分别为(6.54±0.17),(4.36±0.22),(5.51±0.19),(4.86±0.12)nmol/mL,明显低于模型组的(14.15±0.29)nmol/mL(P<0.05).海兔素中剂量组及维生素E对照组小鼠血清中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性比模型组升高(P<0.05).结论 海兔素可有效降低H2O2诱导的DNA氧化损伤和减少DNA烷化损伤产物O6-MeG的生成,提高血清中SOD、GSH-Px活性,降低血清中MDA含量,具有一定的抗氧化作用.     

苹果多酚对D-半乳糖致衰小鼠衰老的影响

<正>苹果多酚是苹果中所含多元酚类物质的通称,果皮及未成熟果实中含量较高,粉末状产品于室温下保存一年其性质及生理功能不变[1]。苹果多酚是安全无毒[2]的食品添加剂,具有降血脂抗动脉粥样硬化[3-4]、抗炎[5-6]、抗氧化[7-8]、抗癌[9-10]和抗菌[11-12]等活性。本研究以皮下注射D-半乳糖     

地锦草总黄酮对D-半乳糖衰老模型小鼠抗氧化作用的研究

地锦草为常用的中蒙药材，具有清热解毒、燥黄水、活血等功效，通过现代药理学研究证实地锦草主要含有槲皮素及其甙、山奈素及其甙等黄酮类化合物。本课题组前期研究了地锦草药理学活性，发现其水及乙醇提取物具有良好的抗脂质过氧化等作用，在此基础上，拟研究地锦草总黄酮（TFEH）对D-半乳糖衰老模型小鼠抗氧化作用及其应用前景。     

Cu-Zn SOD活力变化与铝致小鼠神经元退行性变关系

目的观察在铝染毒致小鼠脑神经元退行性变过程中铜锌超氧化物歧化酶(Cu-Zn SOD)活力变化的规律,以分析两者的关系。方法葡萄糖酸铝溶液(按Al3 400 mg/kg剂量)灌胃给予小鼠,1次/d,每周5 d,连续12周。观察小鼠被动回避性学习记忆能力和空间识别能力的改变、脑组织Cu-Zn SOD活力、脑组织丙二醛(MDA)和总蛋白含量的变化,以及海马神经元的病理形态学变化。结果与对照组比较,铝染毒小鼠第6周后跳台潜伏期呈时间依赖性进行性缩短,而水迷宫寻台时间显著延长,大脑皮层和海马Cu-Zn SOD活力呈明显先升高后下降趋势,MDA和蛋白水平持续升高,海马出现进行性神经元核固缩加重和神经元丢失。结论铝染毒导致代表小鼠脑氧化应激的MDA含量增加和代表抗氧化应激反应的Cu-Zn SOD活力增强;两者反应失衡可能与铝染毒致神经元退行性变有关。     

马齿苋提取物对D-半乳糖致衰老的小鼠体内抗氧化效应

<正>马齿苋(Portulaca oleracea L.)又称马齿草、马齿菜、安乐菜,系马齿苋科马齿苋属一年生肉质草本植物。文献报道马齿苋具有抑菌[1]、降血糖作用[2]、耐缺氧[3]等生物活性。宋曙辉等[4]采用黄嘌呤氧化酶-NBT法对20个科60种蔬菜进行了抗氧化作用的研究,结果表明马齿苋的     

女贞子对D-半乳糖致衰老小鼠学习和记忆的影响

目的探讨女贞子对实验性衰老小鼠的抗衰老作用及其机制。方法以D-半乳糖致亚急性衰老小鼠为模型,同时给予女贞子煎剂治疗,6周后,以学习与记忆成绩、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、Na -K -ATP酶、丙二醛(MDA)为指标,评价女贞子延缓衰老的作用。结果在跳台实验中,女贞子高、中、低浓度组的潜伏期(S)(208.7±92.33、205.9±86.5、188.8±90.1)均明显长于衰老对照组(110.2±88.5,P<0.01),高、中浓度组的错误次数(0.9±0.6、1.4±0.7)均明显少于衰老对照组(2.3±0.8,P<0.01,P<0.05)。与衰老对照组比较,女贞子组小鼠脑组织中的SOD、GSH-Px、Na -K -ATP酶活性增加,MDA含量减少。结论女贞子能明显地改善D-半乳糖致衰老小鼠的学习与记忆能力,其作用机制可能与其提高抗氧化酶活性、清除自由基、减少过氧化脂质的生成有关。     

腰椎间盘退行性变研究进展

目前,腰痛有很高的发病率[1],椎间盘退行性变可能是发生慢性腰痛的主要原因之一[2-3].根据组织学和MR检查,我们发现早在20岁时,椎间盘就已经有了退行性变[4-5].最早发生在髓核(nucleus pulposus,NP),以现有细胞的丢失和基质的改变为主.随着病变的进展,纤维环(annulus fibrosus,AF)的外层会改变其正常的层状排列顺序,从而使椎间盘的受力发生改变.久而久之,从AF内部向外部逐渐开始出现裂隙慢慢变为裂口,进而导致了整体性力学改变[6].这些变化增加了传递到椎体终板的力,引起微小的骨折和边缘骨赘形成.产生并刺激血管和神经向椎间盘内部生长的细胞因子在腰痛中也起了重要的作用[7].椎间盘退行性变的程度与腰痛的临床表现之间并没有很大的关系[8].     

乳蛋白活性肽的延缓衰老作用研究

目的：研究乳蛋白活性肽对果蝇寿命和大鼠氧化与抗氧化指标的影响。方法：果蝇生存实验，大鼠抗氧化实验。结果：乳蛋白活性肽可明显延长两个性别果蝇的最高寿命和平均寿命，同时可明显降低大鼠血清中丙二醛（MDA）含量，并显升高大鼠抗氧化酶（超氧化物歧化酶SOD及谷胱甘肽过氧化物酶GSH－Px）的活力。结论：乳蛋白活性肽有延缓衰老作用。     

蜂蜜枸杞番茄汁对D-半乳糖所致衰老小鼠的壮阳作用研究

目的研究蜂蜜枸杞番茄汁对D-半乳糖所致衰老小鼠的壮阳作用。方法取NIH小鼠50只随机分为对照组、模型组、蜂蜜枸杞番茄汁高(24.804g/kg)、中(12.402g/kg)、低(6.201g/kg)剂量组,分别灌胃给样40d。考察蜂蜜枸杞番茄汁对D-半乳糖衰老模型小鼠血清中丙二醛(MDA)水平、超氧化物歧化酶(SOD)活性、血清和睾丸组织中睾酮水平、精液乳酸脱氢酶(LDH)水平以及精子活动率的影响。结果模型组小鼠血清中MDA水平高于对照组,血清中SOD活性、血清及睾丸中睾酮水平、精囊腺中LDH水平及精子活动率低于对照组,差异有统计学意义(P0.05);蜂蜜枸杞番茄汁高剂量组小鼠血清中睾酮水平高于模型组,差异有统计学意义(P0.05);蜂蜜枸杞番茄汁中剂量组小鼠血清中MDA水平低于模型组,SOD活性高于模型组,精囊腺中LDH水平及精子活动率高于模型组,差异有统计学意义(P0.05);蜂蜜枸杞番茄汁低剂量组小鼠血清中SOD活性、血清及睾丸中睾酮水平、精囊腺中精子活动率高于模型组,差异有统计学意义(P0.05)。结论蜂蜜枸杞番茄汁对D-半乳糖所致衰老小鼠具有壮阳作用。     

蔓越莓对衰老小鼠和辐照小鼠抗氧化功能的影响

目的：探讨蔓越莓对小鼠的抗衰老作用及机制，观察其是否能有效地改善机体的抗氧化能力。方法：采用自然衰老和辐照两种模型小鼠分别给予不同剂量的蔓越莓30d，分别测定小鼠血及肝组织中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）的活力和丙二醛（MDA）的含量。结果：蔓越莓能显著增强小鼠血及肝组织中SOD和GSH-Px的活力（P〈O．05）；降低小鼠血及肝组织MDA含量（P〈O．05）。结论：蔓越莓对自然衰老和辐照模型小鼠均有改善机体抗氧化能力。     

The Potential of Calorie Restriction and Calorie Restriction Mimetics in Delaying Aging: Focus on Experimental Models

Aging is a biological process determined by multiple cellular mechanisms, such as genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication, that ultimately concur in the functional decline of the individual. The evidence that the old population is steadily increasing and will triplicate in the next 50 years, together with the fact the elderlies are more prone to develop pathologies such as cancer, diabetes, and degenerative disorders, stimulates an important effort in finding specific countermeasures. Calorie restriction (CR) has been demonstrated to modulate nutrient sensing mechanisms, inducing a better metabolic profile, enhanced stress resistance, reduced oxidative stress, and improved inflammatory response. Therefore, CR and CR-mimetics have been suggested as powerful means to slow aging and extend healthy life-span in experimental models and humans. Taking into consideration the difficulties and ethical issues in performing aging research and testing anti-aging interventions in humans, researchers initially need to work with experimental models. The present review reports the major experimental models utilized in the study of CR and CR-mimetics, highlighting their application in the laboratory routine, and their translation to human research.     

银耳多糖对实验性衰老模型小鼠免疫功能的影响

目的观察银耳多糖对D-半乳糖所致衰老小鼠免疫功能的影响。方法40只雄性ICR小鼠，分为5组，每天腹腔注射D-半乳糖120mg／kg，连续60天，建立亚急性衰老模型；同时A、B、C组每天分别灌胃800、400和200mg／kg银耳多糖。实验结束后，MTT法检测ConA诱导的小鼠脾淋巴细胞增殖转化，ELISA法检测银耳多糖对小鼠血清IL-2和IL-6的影响。结果银耳多糖能明显促进ConA诱导的小鼠淋巴细胞增殖转化；各银耳多糖干预组小鼠血清IL-2和IL-6均高于衰老对照组。结论银耳多糖可以提高D-半乳糖所致衰老小鼠的免疫功能。     

姜黄素对D-半乳糖所致衰老小鼠学习记忆的影响

目的观察姜黄素对D半-乳糖所致衰老小鼠学习记忆障碍的保护作用。方法 50只ICR小鼠,随机分为5组:对照组,阿尔茨海默病(AD)模型组,姜黄素预处理组、同时处理组和后处理组。采用跳台试验和避暗试验方法,观察姜黄素对AD模型小鼠学习记忆障碍的影响。结果行为学试验显示,模型组小鼠潜伏期短,错误次数增多,与对照组比,P<0.05;姜黄素预处理组和同时处理组潜伏期延长,错误次数减少,学习记忆明显改善,与模型组比,P<0.05。结论姜黄素对AD模型小鼠的学习记忆能力减退具有改善作用。     

Anti-Aging Effect of Dietary Fiber Compound Mediated by Guangxi Longevity Dietary Pattern on Natural Aging Mice

A series of previous studies by our team has shown that the Guangxi longevity dietary pattern contributes to the improvement of human health, but the role of dietary fiber compounds (DFC) in the anti-aging of this dietary pattern has not been studied in depth. Thus, mice were fed with 5%, 15%, and 30% of the characteristic dietary fiber compound (CDFC) (compounded according to the longevity dietary pattern) for 8 weeks, and their learning memory capacity, antioxidant capacity, and inflammatory markers, as well as typical microorganisms in the intestinal tract were analyzed to investigate the anti-aging effects of the CDFC under the Guangxi longevity dietary pattern on naturally aging mice. The results showed that CDFC had a bidirectional effect on body weight regulation; increased brain, spleen, and cardiac indices, of which the medium dose was the best. Meanwhile, CDFC also had a maintenance and improvement effect on learning and memory ability in aging mice, as well as improved antioxidant capacity and reduced inflammation level. The neuronal cell necrosis in the hippocampus of mice was effectively alleviated. The expression of Escherichia coli and Bacteroides was significantly reduced, and the expression of Bifidobacterium and Lactobacillus increased. In addition, the optimal amount of CDFC added from the level of experimental animals was in a certain interval above and below 15%. The combined results indicated that CDFC mediated by the Guangxi longevity dietary pattern had significant anti-aging effects, thus theoretically proving that dietary fiber compound contributes to human longevity.     

Effect of High-Oleic Peanut Intake on Aging and Its Hippocampal Markers in Senescence-Accelerated Mice (SAMP8)

In many previous studies, the preventive effects of peanut against aging and cognitive impairment have often been unclear, so to clarify the effects we first investigated effective markers for evaluating its effects in the hippocampus of senescence-accelerated mouse prone/8 (SAMP8) mice, mainly using proteomics. The effects of dietary high-oleic peanuts on the hair appearance of SAMP8, the expression of effective markers in the hippocampus, and the TBARS and amino acid contents of the hippocampus were examined. Hippocampus solute carrier family 1 (glial high-affinity glutamate transporter), calcium/calmodulin-dependent protein kinase type II, and sodium- and chloride-dependent GABA transporter, which all are considered to be closely related to glutamic acid concentration were decreased by feeding of the samples, and the GABA/glutamic acid ratio in the hippocampus was increased by feeding with the samples. The formation of glial fibrillary acidic protein and synapsin-2, which showed higher levels in the SAMP8 than in SAMR1, and the protein expression of tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein and dihydropteridine reductase, which are considered to be related to the formation of adrenergic neuron transmitters, were reduced by the feeding of peanuts and their germ-rich fraction. Ferulic acid, as an ester and minor component in peanuts, could be partly connected to the effect of peanuts. These results indicate that high-oleic peanuts and their germ-rich fraction can protect against aging and cognitive impairment by regulating protein expression, which could be measured by the proteomics of the above hippocampus proteins of SAMP8 and the hippocampal GABA/glutamic acid ratio.     

The Antioxidant Effects of Whey Protein Peptide on Learning and Memory Improvement in Aging Mice Models

This study investigated the antioxidant effects of whey protein peptide on learning and memory in aging C57BL/6N mice. A total of 72 SPF male C57BL/6N mice were used. Twelve mice were randomly selected as the control group, and the other mice were intraperitoneally injected with D-galactose (100 mg/kg body weight for 6 weeks), during which, the mice in the control group were intraperitoneally injected with the same amount of normal saline. After 6 weeks, the blood was taken from the epicanthus and the serum MDA level was measured, according to which, the mice were randomly divided into the model control group, the whey protein group (1.5 g/kg body weight), and three Whey protein peptide (WHP) intervention groups (0.3 g/kg body weight, 1.5 g/kg body weight, 3.0 g/kg body weight). The water solution of the test sample was administered by oral gavage every day. The intervention period was 30 days, during which, the model control group, the whey protein group, and the whey protein peptide group continued receiving intraperitoneal injections of D-galactose, while the control group continued receiving intraperitoneal injections of normal saline. After the intervention, behavioral experiments were conducted in the following order: open field test, water maze test, and new object recognition test. After the behavioral experiment, the morphology of hippocampal formation was observed by HE staining and TUNEL labeling. Oxidative stress-related indexes in the serum, liver, and brain were detected. Expression levels of the cholinergic system-related enzymes and proinflammatory cytokines in brain tissue were detected. Western blot was used to detect the expression of synaptic plasticity-related proteins in the mouse brain. The results showed that WHP could significantly improve the accumulation of MDA and PC, increase the activities of SOD and GSH-Px, resist oxidative stress injury, and enhance the potential of endogenous antioxidant defense mechanisms. WHP can significantly improve the decline of aging-related spatial exploration, body movement, and spatial and non-spatial learning/memory ability. Its specific mechanism may be related to reducing the degeneration of hippocampal nerve cells, reducing the apoptosis of nerve cells, improving the activity of AChE, reducing the expression of inflammatory factors (TNF-α and IL-1β) in brain tissue, reducing oxidative stress injury, and improving the expression of p-CaMKⅡ and BDNF synaptic plasticity protein. These results indicate that WHP can improve aging-related oxidative stress, as well as learning and memory impairment.