褪黑素与衰老

随年龄增长松果腺功能减退、褪黑素分泌降低。施用ＭＴ或松果腺移植可使机体寿命延长。本文从ＭＴ抗氧化、增强免疫和调整生物钟功能等方面,阐明ＭＴ延缓衰老作用的机理。     

植物叶片衰老及其延缓的分子途径

综述了植物叶片衰老过程中基因表达的上调和下调两种趋势,以及与转ｉｐｔ基因研究有关的问题：（１）ＣＴＫ／ＩＡＡ平衡;（２）形态发育;（３）抗衰老作用;（４）启动子选择等。     

衰老能延缓吗？

衰老是生命的基本现象。纵观古今中外，无论帝王将相、骚人墨客，还是凡夫俗子，概莫能外。既求长生，又求不老，两者岂能兼得？难乎哉!白居易的乐府说出了这种尴尬：“生若不足恋，老也何足悲。生若苟可恋，老即多生时。不老即须天，不天即须衰。既衰胜早天，此理决不疑。”他劝大家宁可忍受衰老，也切莫早天，说白了不就是好死不如赖活吗!但今非昔比，科学的进步使人不满足于赖活，难道我们就找不到让人既活得好，又活得长的办法吗？     

人体衰老与延缓衰老

<正>衰老是自然规律[1],是人体在生长发育达到成熟后,生理结构和功能等所表现的一系列退行性变化[2],但衰老是可以延缓的。现就人体衰老的原因及延缓衰老的对策简述如下。1机体细胞学的分裂传代生物的寿命是靠组织细胞分裂传代(衰老的细胞由分裂新生成熟所代替),但每传一代的线粒体都比原来短(端粒酶),当短到不能计数生命就停止。人体可分裂传代的组织     

延缓衰老有办法

尽管人类不可避免地会死亡,但是未来人类的衰老过程却有办法变慢,寿命也会明显延长。科学家们对人类衰老的生物、化学过程提出了新的解释,为延年益寿药物的问世敞开了大门。虽然他们的研究方法不是完全相同,但有一个共同的认识:人类的寿命并不是固定不变的。     

双歧啤酒对延缓衰老作用的研究

目的研究双歧啤酒的延缓衰老作用。方法将老龄小鼠和黑腹果蝇随机分成纯净水对照组、市售啤酒对照组和双歧啤酒低、中、高三个剂量组,进行果蝇生存实验,检测小鼠血液中超氧化物歧化酶（SOD）、谷光甘肽过氧化物酶（GSH-PX）的活性和丙二醛（MDA）的含量。结果与对照组比较,双歧啤酒高、中剂量组能显著延长果蝇的半数死亡时间、平均寿命和平均最高寿命,提高老龄小鼠血液中SOD、GSH-PX的活性,降低老龄小鼠血液中MDA的含量。结论双歧啤酒具有延缓衰老的作用。     

褪黑素调节卵巢功能及相关机制的研究进展

褪黑素是一种神经内分泌激素,在动物体内主要由松果体合成和分泌,具有调节昼夜节律的重要作用,包括卵巢生物钟系统.褪黑素在外周组织器官如女性生殖器官卵巢中也发挥重要生理作用.女性生殖过程中,卵泡不断产生并累积活性氧,进而造成组织细胞损伤.褪黑素可通过受体依赖或者受体非依赖的机制参与卵巢功能调节.最近研究发现,褪黑素还可通过...     

水杨酸延缓离体爬山虎叶片衰老的作用

爬山虎是修饰藤架和墙体的绿化垂体观赏植物,延缓爬山虎叶片衰老可延长爬山虎绿叶的观赏期.本文探讨了水杨酸(salicylic acid,SA)延缓叶片衰老的作用.     

Sonic hedgehog promotes neurite outgrowth of cortical neurons under oxidative stress: Involving of mitochondria and energy metabolism

Oxidative stress has been demonstrated to be involved in the etiology of several neurobiological disorders. Sonic hedgehog (Shh), a secreted glycoprotein factor, has been implicated in promoting several aspects of brain remodeling process. Mitochondria may play an important role in controlling fundamental processes in neuroplasticity. However, little evidence is available about the effect and the potential mechanism of Shh on neurite outgrowth in primary cortical neurons under oxidative stress. Here, we revealed that Shh treatment significantly increased the viability of cortical neurons in a dose-dependent manner, which was damaged by hydrogen peroxide (H₂O₂). Shh alleviated the apoptosis rate of H₂O₂-induced neurons. Shh also increased neuritogenesis injuried by H₂O₂ in primary cortical neurons. Moreover, Shh reduced the generation of reactive oxygen species (ROS), increased the activities of SOD and and decreased the productions of MDA. In addition, Shh protected mitochondrial functions, elevated the cellular ATP levels and amelioratesd the impairment of mitochondrial complex II activities of cortical neurons induced by H₂O₂. In conclusion, all these results suggest that Shh acts as a prosurvival factor playing an essential role to neurite outgrowth of cortical neuron under H₂O₂ -induced oxidative stress, possibly through counteracting ROS release and preventing mitochondrial dysfunction and ATP as well as mitochondrial complex II activities against oxidative stress.     

Energy Stress-Induced Dopamine Loss in Glutathione Peroxidase-Overexpressing Transgenic Mice and in Glutathione-Depleted Mesencephalic Cultures

Abstract: The role of the glutathione system in protecting dopamine neurons from a mild impairment of energy metabolism imposed by the competitive succinate dehydrogenase inhibitor, malonate, was investigated in vitro and in vivo. Treatment of mesencephalic cultures with 10 µ M buthionine sulfoxamine for 24 h reduced total glutathione levels in the cultures by 68%. Reduction of cellular glutathione per se was not toxic to the dopamine population, but potentiated toxicity when the cultures were exposed to malonate. In contrast, transgenic mice overexpressing glutathione peroxidase (hGPE) that received an intrastriatal infusion of malonate (3 µmol) into the left side had significantly less loss of striatal dopamine than their hGPE-negative littermates when assayed 1 week following infusion. These studies demonstrate that manipulation of the glutathione system influences susceptibility of dopamine neurons to damage due to energy impairment. The findings may provide insight into the loss of dopamine neurons in Parkinson's disease in which defects in both energy metabolism and the glutathione system have been identified.     

Assessment of chronological lifespan dependent molecular damages in yeast lacking mitochondrial antioxidant genes

The free radical theory of aging states that oxidative damage to biomolecules causes aging and that antioxidants neutralize free radicals and thus decelerate aging. Mitochondria produce most of the reactive oxygen species, but at the same time have many antioxidant enzymes providing protection from these oxidants. Expecting that cells without mitochondrial antioxidant genes would accumulate higher levels of oxidative damage and, therefore, will have a shorter lifespan, we analyzed oxidative damages to biomolecules in young and chronologically aged mutants lacking the mitochondrial antioxidant genes: GRX2, CCP1, SOD1, GLO4, TRR2, TRX3, CCS1, SOD2, GRX5, and PRX1. Among these mutants, ccp1Δ, trx3Δ, grx5Δ, prx1Δ, mutants were sensitive to diamide, and ccs1Δ and sod2Δ were sensitive to both diamide and menadione. Most of the mutants were less viable in stationary phase. Chronologically aged cells produced higher amount of superoxide radical and accumulated higher levels of oxidative damages. Even though our results support the findings that old cells harbor higher amount of molecular damages, no significant difference was observed between wild type and mutant cells in terms of their damage content.     

Circadian rhythms of oxidative phosphorylation: effects of rotenone and melatonin on isolated rat brain mitochondria

Mitochondrial experiments are of increasing interest in different fields of research. Inhibition of mitochondrian activities seems to play a role in Parkinson's disease and in this regard several animal models have used inhibitors of mitochondrial respiration such as rotenone or MPTP. Most of these experiments were done during the daytime. However, there is no reason for mitochondrial respiration to be constant during the 24h. This study investigated the circadian variation of oxidative phosphorylation in isolated rat brain mitochondria and the administration-time-dependent effect of rotenone and melatonin. The respiratory control ratio, state 3 and state 4, displayed a circadian fluctuation. The highest respiratory control ratio value (3.01) occurred at 04:00h, and the lowest value (2.63) at 08:00h. The highest value of state 3 and state 4 oxidative respiration occurred at 12:00h and the lowest one at 20:00h. The 24h mean decrease in the respiratory control ratio following incubation with melatonin and rotenone was 7 and 32%, respectively; however, the exact amount of the inhibition exerted by these agents varied according to the time of the mitochondria isolation. Our results show the time of mitochondrial isolation could lead to interindividual variability. When studies require mitochondrial isolation from several animals, the time between animal experiments has to be minimized. In oxidative phosphorylation studies, the time of mitochondria isolation must be taken into account, or at least specified in the methods section.     

Circadian Rhythms of Oxidative Phosphorylation: Effects of Rotenone and Melatonin on Isolated Rat Brain Mitochondria

Mitochondrial experiments are of increasing interest in different fields of research. Inhibition of mitochondrian activities seems to play a role in Parkinson's disease and in this regard several animal models have used inhibitors of mitochondrial respiration such as rotenone or MPTP. Most of these experiments were done during the daytime. However, there is no reason for mitochondrial respiration to be constant during the 24h. This study investigated the circadian variation of oxidative phosphorylation in isolated rat brain mitochondria and the administration-time-dependent effect of rotenone and melatonin. The respiratory control ratio, state 3 and state 4, displayed a circadian fluctuation. The highest respiratory control ratio value (3.01) occurred at 04:00h, and the lowest value (2.63) at 08:00h. The highest value of state 3 and state 4 oxidative respiration occurred at 12:00h and the lowest one at 20:00h. The 24h mean decrease in the respiratory control ratio following incubation with melatonin and rotenone was 7 and 32%, respectively; however, the exact amount of the inhibition exerted by these agents varied according to the time of the mitochondria isolation. Our results show the time of mitochondrial isolation could lead to interindividual variability. When studies require mitochondrial isolation from several animals, the time between animal experiments has to be minimized. In oxidative phosphorylation studies, the time of mitochondria isolation must be taken into account, or at least specified in the methods section.     

脑能量代谢与线粒体功能关系的研究进展

线粒体是人体内的能量代谢工厂,而脑是人体内能量代谢最活跃的部位。神经元和胶质细胞是脑内主要的细胞。本文对线粒体在能量产生的作用进行综述,同时比较神经元和星形胶质细胞能量代谢的异同及密切联系,并对神经退行性变中能量代谢障碍与线粒体可塑性改变进行了回顾。以三种神经退行性疾病帕金森、阿尔兹海默和脊髓侧索硬化症为例说明线粒体在神经系统疾病和脑能量代谢之间的重要作用。从而进一步系统的认识,脑内的线粒体在生理和病理状态下对能量代谢的影响。深入了解其机制,为研究神经系统退行性疾病提供新的治疗策略。     

急性低氧/复氧胁迫对克氏原螯虾抗氧化-能量代谢的影响

为研究低氧/复氧胁迫对克氏原螯虾(Procambarus clarkii)抗氧化及能量代谢的影响, 将克氏原螯虾暴露于(1.0±0.1) mg/L急性低氧胁迫和后续(6.8±0.2) mg/L复氧环境中, 于低氧胁迫1h、6h及复氧1h、12h分别采集肝胰腺、鳃和血淋巴, 研究低氧/复氧胁迫下克氏原螯虾抗氧化-能量代谢酶的活力变化, 分析鳃和肝胰腺组织的超微结构改变。在低氧胁迫下, 肝胰腺和血淋巴中SOD酶活力显著下降(P<0.05); 复氧以后, 肝胰腺、血淋巴及鳃组织中SOD酶活力均出现了显著上升(P<0.05)。SOD酶活力变化可能与复氧过程中超氧阴离子自由基的过量产生有关。在复氧12h后, 血淋巴和鳃组织中MDA含量均出现了显著性增加(P<0.01), 提示机体细胞在复氧胁迫下产生了脂质过氧化。在低氧胁迫下, 肝胰腺、鳃和血淋巴中ACP、AKP酶活力显著上升(P<0.05); 在复氧12h后, 肝胰腺和鳃组织中ACP酶活力显著降低(P<0.01)。显示低氧/复氧胁迫影响了机体的非特异性免疫应答。在急性低氧胁迫下, 肝胰腺、血淋巴与鳃组织中的LDH含量和总ATPase活力均显著升高(P<0.05), 提示这些组织中的细胞能量代谢功能受到了严重影响。在急性低氧/复氧胁迫下, 肝胰腺及鳃组织中的线粒体结构呈现明显浓缩空泡化、内膜排列紊乱, 嵴明显减少、部分嵴消失。在低氧状态下, 肝胰腺细胞中线粒体数量明显增多, 细胞中溶酶体数量明显减少。结果表明, 低氧/复氧胁迫可对克氏原螯虾造成氧化应激损伤, 对机体非特异性免疫防御及能量代谢功能产生了不利影响, 建议在克氏原螯虾养殖生产中特别关注水体中的低氧/复氧胁迫问题。     

不同类型神经细胞对低氧的敏感性研究*

Objective: In order to illustrate the hypoxia-induced changes of neural cells in inflammatory response, oxidative stress, and energy metabolism process and to compare the sensitivity of neural cells’ responses to hypoxia. Methods: Different types of neural cells (BV2, N9, Gl261, HT22) were treated with hypoxia (0.1% O₂, 5% CO₂) for 0-24 hours. Cell proliferation was detected by Cell Counting Kit-8 method and cell viability was assayed by CellTiter-Glo Luminescent Cell Viability Assay. Total RNA was extracted by Trizol reagent, and the inflammation, oxidative stress, and energy metabolism-related genes expression were measured by quantitative real-time PCR and Western blot. The ROS production was detected by flow cytometer with fluorescence probe. Results: Hypoxia stimulation decreased cell proliferation and cell viability. The hypoxia-induced changes of microglial cells (BV2 and N9) were mainly involved in inflammatory response and glucose metabolism process. The changes of astrocytes Gl261 and neural cell HT22 were mainly involved in glucose metabolism process. Hypoxia stimulation significantly increased oxidative stress in microglia and astrocytes. Conclusion: Different types of neural cells have different degrees of sensitivity in response to hypoxic stimulation. In terms of energy metabolism and inflammatory response, microglia are more sensitive to hypoxia treatment, which is manifested as a significant up-regulation of glycolytic enzymes and inflammation genes, whereas microglia and astrocytes are more sensitive to hypoxia treatment in terms of oxidative stress, which is indicated by their quick response and significant increase of ROS production.     

氧化应激研究进展及其在缺血性心肌病发病中的作用

缺血性心肌病(ischemic cardiomyopathy,ICM)是指由于长期心肌缺血导致心肌局限性或弥漫性纤维化,从而产生心脏收缩和(或)舒张功能受损,引起心脏扩大或僵硬、充血性心力衰竭、心律失常等一系列临床表现的临床综合症。大量研究表明,ICM的发病机制与氧化应激密切相关。研究和开发新的抗氧化药物,将为缺血性心肌病的防治提供新的方向和途径。