Open AccessUrsolic acid improves the indoxyl sulfate-induced impairment of mitochondrial biogenesis in C2C12 cells
Author(s) -
Yutaro Sasaki,
Akiko KojimaYuasa,
Hinako Tadano,
Ayaka Mizuno,
Atsushi Kon,
Toshio Norikura
Publication year - 2022
Publication title -
nutrition research and practice
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.506
H-Index - 34
eISSN - 2005-6168
pISSN - 1976-1457
DOI - 10.4162/nrp.2022.16.2.147
Subject(s) - mitochondrial biogenesis , tfam , fis1 , mfn2 , nrf1 , mitochondrial fusion , mitochondrion , c2c12 , chemistry , myocyte , endocrinology , medicine , biology , microbiology and biotechnology , biochemistry , mitochondrial dna , myogenesis , gene
Patients with chronic kidney disease (CKD) have a high concentration of uremic toxins in their blood and often experience muscle atrophy. Indoxyl sulfate (IS) is a uremic toxin produced by tryptophan metabolism. Although an elevated IS level may induce muscle dysfunction, the effect of IS on physiological concentration has not been elucidated. Additionally, the effects of ursolic acid (UA) on muscle hypertrophy have been reported in healthy models; however, it is unclear whether UA ameliorates muscle dysfunction associated with chronic diseases, such as CKD. Thus, this study aimed to investigate whether UA can improve the IS-induced impairment of mitochondrial biogenesis.