目的:探讨长期有氧运动干预对脑衰老过程中大鼠学习记忆能力以及海马脑源性神经营养因子(BDNF)表达的影响。方法:将30只3月龄SD雄性大鼠随机分成青年对照组(YC组)、衰老对照组(OC组)和衰老运动组(OS组)3组,每组10只。OC组和OS组腹腔注...目的:探讨长期有氧运动干预对脑衰老过程中大鼠学习记忆能力以及海马脑源性神经营养因子(BDNF)表达的影响。方法:将30只3月龄SD雄性大鼠随机分成青年对照组(YC组)、衰老对照组(OC组)和衰老运动组(OS组)3组,每组10只。OC组和OS组腹腔注射D-半乳糖100 mg/kg/d,持续6周,OS组同期每日进行1小时游泳运动。6周后用Morris水迷宫实验评估各组大鼠的学习与记忆能力;然后断头取大鼠海马,分别采用Real Time-PCR和Western Blot技术检测其BDNF m RNA和BDNF蛋白的表达水平;取大脑皮质,进行自由基指标检测。结果:在Morris水迷宫定位航行试验中,与YC组相比,OC组平均逃避潜伏期显著延长(P<0.01);与OC组相比,OS组平均逃避潜伏期缩短(P<0.01)。在空间探索实验中,OC组平均穿越平台区域次数显著性少于YC组与OS组(P<0.01,P<0.05)。OC组海马BNDF m RNA和BNDF蛋白表达水平均低于YC组(P<0.01,P<0.05),而OS组海马BNDF m RNA和BNDF蛋白表达水平高于OC组(P<0.01,P<0.05)。结论:衰老过程中进行有氧运动可延缓脑衰老引起的学习记忆能力下降。有氧运动可上调衰老过程中大鼠海马BDNF的表达,这可能是有氧运动延缓脑衰老、改善学习记忆能力的分子机制之一。展开更多
Inflammation may play a role in postoperative cognitive dysfunction. 5' Adenosine monophos- phate-activated protein kinase, nuclear factor-kappa B, interleukin-1β, and tumor necrosis factor-a are involved in inflamm...Inflammation may play a role in postoperative cognitive dysfunction. 5' Adenosine monophos- phate-activated protein kinase, nuclear factor-kappa B, interleukin-1β, and tumor necrosis factor-a are involved in inflammation. Therefore, these inflammatory mediators may be involved in postoperative cognitive dysfunction. Western immunoblot analysis revealed 5' adenosine mo- nophosphate-activated protein kinase and nuclear factor-kappa B in the hippocampus of aged rats were increased 1-7 days after splenectomy. Moreover, interleukin-1β and tumor necrosis fac- tor-α were upregulated and gradually decreased. Therefore, these inflammatory mediators may participate in the splenectomy model of postoperative cognitive dysfunction in aged rats.展开更多
The present study established a model of brain ischemia in aged rats using four-vessel occlusion.We observed hippocampal CA1 neuronal apoptosis and apoptosis-mediated protease caspase-3 expression following preconditi...The present study established a model of brain ischemia in aged rats using four-vessel occlusion.We observed hippocampal CA1 neuronal apoptosis and apoptosis-mediated protease caspase-3 expression following preconditioning of electroacupuncture at Baihui(GV 20).Our results showed that the number of hippocampal CA1 normal neurons was decreased,and degenerated neurons were increased 12 hours to 3 days following cerebral ischemia/reperfusion.The number of hippocampal CA1 apoptotic neurons and caspase-3-positive neurons in rats with cerebral ischemia/reperfusion injury was significantly decreased following acupuncture preconditioning.Acupuncture preconditioning protects aged rats against ischemia/reperfusion injury by regulating caspase-3 protein expression.展开更多
了解年老过程中大脑在细胞水平上发生的变化对于揭示老年人认知功能下降的原因有重要意义。扩散MRI(diffusion MRI,d MRI)技术是目前惟一可以无创探查活体组织微观结构的方法。扩散张量成像(DTI,diffusion tensor imaging)是临床上最常...了解年老过程中大脑在细胞水平上发生的变化对于揭示老年人认知功能下降的原因有重要意义。扩散MRI(diffusion MRI,d MRI)技术是目前惟一可以无创探查活体组织微观结构的方法。扩散张量成像(DTI,diffusion tensor imaging)是临床上最常用的一种d MRI技术,但是由于某些固有缺陷,它不能充分刻画大脑组织的微观结构。作者介绍三种可以有效弥补DTI不足的新型扩散成像方法:扩散峰度成像(diffusion kurtosis imaging,DKI),扩散的受阻受限合成模型(composite hindered and restricted model of diffusion,CHARMED)和神经突方向离散度与密度成像(neurite orientation dispersion and density imaging,NODDI)。联合使用DTI和这些新技术,研究者可以更深入地了解年老如何影响大脑的微观结构。展开更多
Interleukin-1βis a potent proinflammatory cytokine that plays a key role in the pathogenesis of the brain aging and diverse range of neurological diseases including Alzheimer’s disease,Parkinson’s disease,stroke an...Interleukin-1βis a potent proinflammatory cytokine that plays a key role in the pathogenesis of the brain aging and diverse range of neurological diseases including Alzheimer’s disease,Parkinson’s disease,stroke and persistent pain.Activated microglia are the main cellular source of interleukin-1βin the brain.Cathepsin B is associated with the production and secretion of interleukin-1βthrough pyrin domain-containing protein 3 inflammasome-independent processing of procaspase-3 in the phagolysosomes.The leakage of cathepsin B from the endosomal-lysosomal system during aging is associated with the proteolytic degradation of mitochondrial transcription factor A,which can stabilize mitochondrial DNA.Therefore,microglial cathepsin B could function as a major driver for inflammatory brain diseases and brain aging.Orally active and blood-brain barrier-permeable specific inhibitors for cathepsin B can be potentially effective new pharmaceutical interventions against inflammatory brain diseases and brain aging.展开更多
文摘目的:探讨长期有氧运动干预对脑衰老过程中大鼠学习记忆能力以及海马脑源性神经营养因子(BDNF)表达的影响。方法:将30只3月龄SD雄性大鼠随机分成青年对照组(YC组)、衰老对照组(OC组)和衰老运动组(OS组)3组,每组10只。OC组和OS组腹腔注射D-半乳糖100 mg/kg/d,持续6周,OS组同期每日进行1小时游泳运动。6周后用Morris水迷宫实验评估各组大鼠的学习与记忆能力;然后断头取大鼠海马,分别采用Real Time-PCR和Western Blot技术检测其BDNF m RNA和BDNF蛋白的表达水平;取大脑皮质,进行自由基指标检测。结果:在Morris水迷宫定位航行试验中,与YC组相比,OC组平均逃避潜伏期显著延长(P<0.01);与OC组相比,OS组平均逃避潜伏期缩短(P<0.01)。在空间探索实验中,OC组平均穿越平台区域次数显著性少于YC组与OS组(P<0.01,P<0.05)。OC组海马BNDF m RNA和BNDF蛋白表达水平均低于YC组(P<0.01,P<0.05),而OS组海马BNDF m RNA和BNDF蛋白表达水平高于OC组(P<0.01,P<0.05)。结论:衰老过程中进行有氧运动可延缓脑衰老引起的学习记忆能力下降。有氧运动可上调衰老过程中大鼠海马BDNF的表达,这可能是有氧运动延缓脑衰老、改善学习记忆能力的分子机制之一。
文摘Inflammation may play a role in postoperative cognitive dysfunction. 5' Adenosine monophos- phate-activated protein kinase, nuclear factor-kappa B, interleukin-1β, and tumor necrosis factor-a are involved in inflammation. Therefore, these inflammatory mediators may be involved in postoperative cognitive dysfunction. Western immunoblot analysis revealed 5' adenosine mo- nophosphate-activated protein kinase and nuclear factor-kappa B in the hippocampus of aged rats were increased 1-7 days after splenectomy. Moreover, interleukin-1β and tumor necrosis fac- tor-α were upregulated and gradually decreased. Therefore, these inflammatory mediators may participate in the splenectomy model of postoperative cognitive dysfunction in aged rats.
基金the Science and Technology Bureau of South District of Qingdao, No. 2008041
文摘The present study established a model of brain ischemia in aged rats using four-vessel occlusion.We observed hippocampal CA1 neuronal apoptosis and apoptosis-mediated protease caspase-3 expression following preconditioning of electroacupuncture at Baihui(GV 20).Our results showed that the number of hippocampal CA1 normal neurons was decreased,and degenerated neurons were increased 12 hours to 3 days following cerebral ischemia/reperfusion.The number of hippocampal CA1 apoptotic neurons and caspase-3-positive neurons in rats with cerebral ischemia/reperfusion injury was significantly decreased following acupuncture preconditioning.Acupuncture preconditioning protects aged rats against ischemia/reperfusion injury by regulating caspase-3 protein expression.
文摘了解年老过程中大脑在细胞水平上发生的变化对于揭示老年人认知功能下降的原因有重要意义。扩散MRI(diffusion MRI,d MRI)技术是目前惟一可以无创探查活体组织微观结构的方法。扩散张量成像(DTI,diffusion tensor imaging)是临床上最常用的一种d MRI技术,但是由于某些固有缺陷,它不能充分刻画大脑组织的微观结构。作者介绍三种可以有效弥补DTI不足的新型扩散成像方法:扩散峰度成像(diffusion kurtosis imaging,DKI),扩散的受阻受限合成模型(composite hindered and restricted model of diffusion,CHARMED)和神经突方向离散度与密度成像(neurite orientation dispersion and density imaging,NODDI)。联合使用DTI和这些新技术,研究者可以更深入地了解年老如何影响大脑的微观结构。
基金founded by JSPS KAKENHI,No.24390416,JP15H05015,15K15684 and JP16H01304(all to HN)
文摘Interleukin-1βis a potent proinflammatory cytokine that plays a key role in the pathogenesis of the brain aging and diverse range of neurological diseases including Alzheimer’s disease,Parkinson’s disease,stroke and persistent pain.Activated microglia are the main cellular source of interleukin-1βin the brain.Cathepsin B is associated with the production and secretion of interleukin-1βthrough pyrin domain-containing protein 3 inflammasome-independent processing of procaspase-3 in the phagolysosomes.The leakage of cathepsin B from the endosomal-lysosomal system during aging is associated with the proteolytic degradation of mitochondrial transcription factor A,which can stabilize mitochondrial DNA.Therefore,microglial cathepsin B could function as a major driver for inflammatory brain diseases and brain aging.Orally active and blood-brain barrier-permeable specific inhibitors for cathepsin B can be potentially effective new pharmaceutical interventions against inflammatory brain diseases and brain aging.