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Calorie restriction and stroke

机译:热量限制和中风

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摘要

Stroke, a major cause of disability and mortality in the elderly, occurs when a cerebral blood vessel is occluded or ruptured, resulting in ischemic damage and death of brain cells. The injury mechanism involves metabolic and oxidative stress, excitotoxicity, apoptosis and inflammatory processes, including activation of glial cells and infiltration of leukocytes. In animal models, dietary energy restriction, by daily calorie reduction (CR) or intermittent fasting (IF), extends lifespan and decreases the development of age-related diseases. Dietary energy restriction may also benefit neurons, as suggested by experimental evidence showing that CR and IF protect neurons against degeneration in animal models. Recent findings by our group and others suggest the possibility that dietary energy restriction may protect against stroke induced brain injury, in part by inducing the expression of neurotrophic factors, such as brain-derived neurotrophic factor (BDNF) and basic fibroblast growth factor (bFGF); protein chaperones, including heat shock protein 70 (Hsp70) and glucose regulated protein 78 (GRP78); antioxidant enzymes, such as superoxide dismutases (SOD) and heme oxygenase-1 (HO-1), silent information regulator T1 (SIRT1), uncoupling proteins and anti-inflammatory cytokines. This article discusses the protective mechanisms activated by dietary energy restriction in ischemic stroke.
机译:中风是老年人致残和死亡的主要原因,是在大脑血管闭塞或破裂时发生的,导致缺血性损伤和脑细胞死亡。损伤机制涉及代谢和氧化应激,兴奋性毒性,细胞凋亡和炎症过程,包括神经胶质细胞的活化和白细胞的浸润。在动物模型中,通过每日减少卡路里(CR)或间歇禁食(IF)限制饮食能量,可以延长寿命并减少与年龄有关的疾病的发展。饮食能量限制也可能有益于神经元,如实验证据表明,CR和IF在动物模型中可保护神经元免于变性。我们小组和其他研究人员的最新发现表明,饮食能量限制可能通过预防神经营养因子(如脑源性神经营养因子(BDNF)和碱性成纤维细胞生长因子(bFGF))的表达来预防中风引起的脑损伤;蛋白伴侣,包括热激蛋白70(Hsp70)和葡萄糖调节蛋白78(GRP78);抗氧化剂酶,例如超氧化物歧化酶(SOD)和血红素加氧酶-1(HO-1),沉默信息调节剂T1(SIRT1),解偶联蛋白和抗炎细胞因子。本文讨论了饮食能量限制对缺血性中风激活的保护机制。

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