Dihydromyricetin Improves Hypobaric Hypoxia-Induced Memory Impairment via Modulation of SIRT3 Signaling
Dihydromyricetin Improves Hypobaric Hypoxia-Induced Memory Impairment via Modulation of SIRT3 Signaling
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DOI：
10.1007/s12035-015-9627-y
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发表时间：
2016-12-01
影响因子：
5.1
通讯作者：
Mi, Mantian
中科院分区：
文献类型：
--
作者：
Liu, Peng;Zou, Dan;Mi, Mantian
氧气供应不足——比如在高海拔地区——会导致海马神经退化和记忆障碍。虽然氧化应激是一个因素，但低氧缺氧（HH）影响的机制尚不清楚，预防由此产生的脑损伤的有效策略也有限。在本研究中，我们证明了摄取二氢杨梅素（DM）可以保护成年大鼠在7天的HH中，相当于海拔5000米的记忆损伤。此外，DM治疗刺激线粒体生物发生，改善线粒体形态和功能，抑制活性氧的产生，减少海马脂质过氧化。在暴露于缺氧条件下的HT-22细胞中，DM的神经保护作用是通过sirtuin 3诱导的叉头盒O3去乙酰化来减弱氧化应激。
Inadequate oxygen availability-for instance at high altitudes-leads to hippocampal neurodegeneration and memory impairment. Although oxidative stress is one factor, the mechanism underlying the effects of hypobaric hypoxia (HH) are unclear, and effective strategies for preventing the resultant damage to the brain are limited. In the present study, we demonstrate that ingesting dihydromyricetin (DM) protects against memory impairment in adult rats subjected to HH for 7 days, equivalent to an altitude of 5000 m above sea level. Moreover, DM treatment stimulated mitochondrial biogenesis and improved mitochondrial morphology and function, suppressed the generation of reactive oxygen species, and reduced lipid peroxidation in the hippocampus. In HT-22 cells exposed to hypoxic conditions, the neuroprotective effects of DM were shown to be exerted via attenuation of oxidative stress through sirtuin 3-induced forkhead box O3 deacetylation.