Coenzyme Q10 inhibits RANKL-induced osteoclastogenesis by regulation of mitochondrial apoptosis and oxidative stress in RAW264.7 cells.

Autor: Zheng D; Department of Endocrinology, The Second Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, China., Cui C; The Operative Surgery Laboratory, Bengbu Medical College, Bengbu, Anhui, China., Shao C; Department of Endocrinology, The Second Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, China., Wang Y; Department of Endocrinology, The Second Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, China., Ye C; Department of Endocrinology, The Second Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, China., Lv G; Department of Endocrinology, The Second Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, China.
Jazyk: angličtina
Zdroj: Journal of biochemical and molecular toxicology [J Biochem Mol Toxicol] 2021 Jul; Vol. 35 (7), pp. e22778. Date of Electronic Publication: 2021 Mar 23.
DOI: 10.1002/jbt.22778
Abstrakt: Coenzyme Q10 (CoQ10) has been reported to improve bone density and the number of trabeculae in postmenopausal osteoporosis, but the mechanism remains to be elucidated. We aimed to investigate the effects of CoQ10 on receptor activator of NF-κB ligand (RANKL)-induced osteoclastogenesis and the underlying molecular mechanisms. RAW264.7 cells were treated with different concentrations of RANKL to differentiate into osteoclasts, and then these cells were treated with different concentrations of CoQ10 with or without H 2 O 2 . Tartrate-resistant acid phosphatase staining was performed to detect osteoclasts. Cell viability was tested by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, cell apoptosis was examined by flow cytometry, and the effects of CoQ10 on protein and messenger RNA expression of mitochondrial apoptosis-associated proteins and osteoclast marker proteins were measured by quantitative reverse transcription polymerase chain reaction and western blot, respectively. Furthermore, enzyme-linked immunosorbent assay was conducted to analyze the activities of malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT). RANKL significantly induced osteoclastogenesis in RAW264.7 cells, with the greatest efficiency at 50 ng/ml. CoQ10 had no significant effects on cell viability but it significantly increased the percentages of cell apoptosis. Mechanically, CoQ10 statistically decreased the levels of Bcl-2 and cytochrome C in mitochondria and upregulated the levels of Bax, cleaved caspase 3, and cytochrome C in the cytoplasm. Moreover, CoQ10 significantly decreased RANKL-induced osteoclastogenesis regardless of exposure to H 2 O 2 . In addition, CoQ10 statistically reduced MDA activity and elevated the activities of SOD and CAT, as well as the expression of oxidative stress-related proteins. CoQ10 may inhibit RANKL-induced osteoclastogenesis by regulation of mitochondrial apoptosis and oxidative stress in RAW264.7 cells.
(© 2021 Wiley Periodicals LLC.)
Databáze: MEDLINE
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