{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T14:58:23Z","timestamp":1787065103828,"version":"build-2736575974"},"reference-count":49,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2021,3,23]],"date-time":"2021-03-23T00:00:00Z","timestamp":1616457600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Biochem &amp; Molecular Tox"],"published-print":{"date-parts":[[2021,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    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\u2010\u03baB ligand (RANKL)\u2010induced 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\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    . Tartrate\u2010resistant acid phosphatase staining was performed to detect osteoclasts. Cell viability was tested by 3\u2010(4,5\u2010dimethylthiazol\u20102\u2010yl)\u20102,5\u2010diphenyltetrazolium bromide assay, cell apoptosis was examined by flow cytometry, and the effects of CoQ10 on protein and\u00a0messenger RNA expression of mitochondrial apoptosis\u2010associated proteins and osteoclast marker proteins were measured by quantitative reverse transcription polymerase chain reaction and western blot, respectively. Furthermore,\u00a0enzyme\u2010linked 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\u2009ng\/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\u20102 and cytochrome\n                    <jats:italic>C<\/jats:italic>\n                    in mitochondria and upregulated the levels of Bax, cleaved caspase 3, and cytochrome\n                    <jats:italic>C<\/jats:italic>\n                    in the cytoplasm. Moreover, CoQ10 significantly decreased RANKL\u2010induced osteoclastogenesis regardless of exposure to H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    . In addition, CoQ10 statistically reduced MDA activity\u00a0and elevated the activities of SOD and CAT, as well as\u00a0the expression of oxidative stress\u2010related proteins. CoQ10 may inhibit RANKL\u2010induced osteoclastogenesis by regulation of mitochondrial apoptosis and oxidative stress in RAW264.7 cells.\n                  <\/jats:p>","DOI":"10.1002\/jbt.22778","type":"journal-article","created":{"date-parts":[[2021,3,23]],"date-time":"2021-03-23T03:15:44Z","timestamp":1616469344000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Coenzyme Q10 inhibits RANKL\u2010induced osteoclastogenesis by regulation of mitochondrial apoptosis and oxidative stress in RAW264.7 cells"],"prefix":"10.1002","volume":"35","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7861-7885","authenticated-orcid":false,"given":"Delu","family":"Zheng","sequence":"first","affiliation":[{"name":"Department of Endocrinology The Second Affiliated Hospital of Bengbu Medical College  Bengbu Anhui China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chenli","family":"Cui","sequence":"additional","affiliation":[{"name":"The Operative Surgery Laboratory, Bengbu Medical College  Bengbu Anhui China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chen","family":"Shao","sequence":"additional","affiliation":[{"name":"Department of Endocrinology The Second Affiliated Hospital of Bengbu Medical College  Bengbu Anhui China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanqiu","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Endocrinology The Second Affiliated Hospital of Bengbu Medical College  Bengbu Anhui China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chengsong","family":"Ye","sequence":"additional","affiliation":[{"name":"Department of Endocrinology The Second Affiliated Hospital of Bengbu Medical College  Bengbu Anhui China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gaoyou","family":"Lv","sequence":"additional","affiliation":[{"name":"Department of Endocrinology The Second Affiliated Hospital of Bengbu Medical College  Bengbu Anhui China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2021,3,23]]},"reference":[{"key":"e_1_2_9_2_1","doi-asserted-by":"publisher","DOI":"10.1055\/s-0038-1660790"},{"key":"e_1_2_9_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00198-019-05173-6"},{"key":"e_1_2_9_4_1","doi-asserted-by":"publisher","DOI":"10.1007\/s11657-020-0685-z"},{"key":"e_1_2_9_5_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrdp.2016.69"},{"issue":"14","key":"e_1_2_9_6_1","first-page":"1869","volume":"17","author":"Evsen M. 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