TFAM公司
线粒体生物发生
柠檬酸合酶
尼泊尔卢比1
线粒体
线粒体DNA
辅活化剂
过氧化物酶体增殖物激活受体
生物
肉碱
PPARGC1A型
DNAJA3公司
细胞器生物发生
细胞生物学
细胞色素c氧化酶
氧化磷酸化
转录因子
内科学
生物化学
受体
生物发生
基因
酶
作者
Vito Pesce,Flavio Fracasso,P Cassano,Angela Maria Serena Lezza,Palmiro Cantatore,Maria Nicola Gadaleta
标识
DOI:10.1089/rej.2009.0955
摘要
The age-related decay of mitochondrial function is a major contributor to the aging process. We tested the effects of 2-month-daily acetyl-L-carnitine (ALCAR) supplementation on mitochondrial biogenesis in the soleus muscle of aged rats. This muscle is heavily dependent on oxidative metabolism. Mitochondrial (mt) DNA content, citrate synthase activity, transcript levels of some nuclear- and mitochondrial-coded genes (cytochrome c oxidase subunit IV [COX-IV], 16S rRNA, COX-I) and of some factors involved in the mitochondrial biogenesis signaling pathway (peroxisome proliferator-activated receptor gamma [PPARgamma] coactivator-1alpha [PGC-1alpha], mitochondrial transcription factor A mitochondrial [TFAM], mitochondrial transcription factor 2B [TFB2]), as well as the protein content of PGC-1alpha were determined. The results suggest that the ALCAR treatment in old rats activates PGC-1alpha-dependent mitochondrial biogenesis, thus partially reverting the age-related mitochondrial decay.
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