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首页> 外文期刊>Aging cell. >Reactive oxygen species, dietary restriction and neurotrophic factors in age-related loss of myenteric neurons.
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Reactive oxygen species, dietary restriction and neurotrophic factors in age-related loss of myenteric neurons.

机译：与年龄相关的肌层神经元丢失的活性氧，饮食限制和神经营养因子。

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We have studied the mechanisms underlying nonpathological age-related neuronal cell death. Fifty per cent of neurons in the rat enteric nervous system are lost between 12 and 18 months of age in ad libitum (AL) fed rats. Caloric restriction (CR) protects almost entirely against this neuron loss. Using the ROS-sensitive dyes, dihydrorhodamine (DHR) and 2-[6-(4'-hydroxy)phenoxy-3H-xanthen-3-on-9-yl]benzoic acid (HPF) in vitro, we show that the onset of cell death is linked with elevated intraneuronal levels of reactive oxygen species (ROS). Treatment with the neurotrophic factors NT3 and GDNF enhances neuronal antioxidant defence in CR rats at 12-15 months and 24 months but not in adult or aged AL-fed animals. To examine the link between elevated ROS and neuronal cell death, we assessed apoptotic cell death following in vitro treatment with the redox-cycling drug, menadione. Menadione fails to increase apoptosis in 6-month neurons. However, in 12-15mAL fed rats, when age-related cell death begins, menadione induces a 7- to 15-fold increase in the proportion of apoptotic neurons. CR protects age-matched neurons against ROS-induced apoptosis. Treatment with neurotrophic factors, in particular GDNF, rescues neurons from menadione-induced cell death, but only in 12-15mCR animals. We hypothesize that CR enhances antioxidant defence through neurotrophic factor signalling, thereby reducing age-related increases in neuronal ROS levels and in ROS-induced cell death.
机译：我们已经研究了与年龄无关的非病理性神经元细胞死亡的机制。在随意喂养（AL）的大鼠中，大鼠肠神经系统中50％的神经元在12至18个月大时丢失。热量限制（CR）几乎完全可以防止这种神经元丢失。在体外使用ROS敏感染料，二氢罗丹明（DHR）和2- [6-（4'-羟基）苯氧基-3H-黄嘌呤-3-on-9-基]苯甲酸（HPF），我们证明了发病细胞死亡的原因与神经内活性氧水平（ROS）升高有关。用神经营养因子NT3和GDNF进行治疗可增强CR大鼠在12-15个月和24个月时的神经元抗氧化防御能力，但不能在成年或成年AL喂养的动物中增强。为了检查ROS升高与神经元细胞死亡之间的联系，我们在用氧化还原循环药物甲萘醌进行体外治疗后评估了凋亡细胞的死亡。甲萘醌不能增加6个月神经元的凋亡。然而，在12-15mAL喂养的大鼠中，当与年龄相关的细胞死亡开始时，甲萘醌诱导凋亡神经元的比例增加7至15倍。 CR保护年龄匹配的神经元免受ROS诱导的细胞凋亡。用神经营养因子，特别是GDNF进行的治疗，可将神经元从甲萘醌诱导的细胞死亡中拯救出来，但仅限于12-15mCR动物。我们假设CR通过神经营养因子信号传导增强抗氧化防御，从而减少与年龄相关的神经元ROS水平增加和ROS诱导的细胞死亡。

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