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硫辛酸补充对年龄和铁诱导的记忆障碍、线粒体 DNA 损伤和抗氧化反应的影响。

Effects of lipoic acid supplementation on age- and iron-induced memory impairment, mitochondrial DNA damage and antioxidant responses.

机构信息

Laboratory of Genomics and Molecular Biology, School of Health and Life Sciences, Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil.

Neurobiology and Developmental Biology Laboratory, Faculty of Biosciences, Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil.

出版信息

Eur J Nutr. 2021 Oct;60(7):3679-3690. doi: 10.1007/s00394-021-02541-z. Epub 2021 Mar 18.

Abstract

PURPOSE

To investigate the effects of lipoic acid (LA) supplementation during adulthood combined with supplementation later in life or LA administration only at old age on age-induced cognitive dysfunction, mitochondrial DNA deletions, caspase 3 and antioxidant response enzymes expression in iron-treated rats.

METHODS

Male rats were submitted to iron treatment (30 mg/kg body wt of Carbonyl iron) from 12 to 14th post-natal days. Iron-treated rats received LA supplementation (50 mg/kg, daily) in adulthood and old age or at old age only for 21 days. Memory, mitochondrial DNA (mtDNA) complex I deletions, caspase 3 mRNA expression and antioxidant response enzymes mRNA expression were analyzed in the hippocampus.

RESULTS

LA administration in adulthood combined with treatment later in life was able to reverse age-induced effects on object recognition and inhibitory avoidance memory, as well as on mtDNA deletions, nuclear factor (erythroid-derived 2)-like 2 (Nrf2) expression, and antioxidant enzymes disruption induced by iron in aged rats. LA treatment only at old age reversed iron-induced effects to a lesser extent when compared to the combined treatment.

CONCLUSION

The present findings support the view that LA supplementation may be considered as an adjuvant against mitochondrial damage and cognitive decline related to aging and neurodegenerative disorders.

摘要

目的

研究成年期补充硫辛酸(LA)并在晚年补充或仅在老年期补充 LA 对铁处理大鼠诱导的年龄相关认知功能障碍、线粒体 DNA 缺失、半胱氨酸蛋白酶 3 和抗氧化反应酶表达的影响。

方法

雄性大鼠从出生后第 12 至 14 天接受铁处理(30mg/kg 体重的羰基铁)。铁处理大鼠在成年期和老年期或仅在老年期接受 LA 补充(50mg/kg,每日)21 天。在海马体中分析记忆、线粒体 DNA(mtDNA)复合物 I 缺失、半胱氨酸蛋白酶 3 mRNA 表达和抗氧化反应酶 mRNA 表达。

结果

成年期补充 LA 并在晚年治疗能够逆转铁处理对老龄大鼠物体识别和抑制性回避记忆以及 mtDNA 缺失、核因子(红细胞衍生 2)样 2(Nrf2)表达和抗氧化酶破坏的年龄诱导作用。与联合治疗相比,老年期仅接受 LA 治疗的效果较小。

结论

本研究结果支持补充 LA 可作为一种辅助治疗,用于对抗与衰老和神经退行性疾病相关的线粒体损伤和认知能力下降。

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