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Osteoclasts are the primary effector cells that degrade bone matrix and their abnormal function leads to the development of osteoporosis. Reactive oxygen species (ROS) accumulation during cellular metabolism promotes osteoclast proliferation and differentiation, therefore, playing an important role in osteoporosis.\n                    <jats:italic>Cistanche deserticola<\/jats:italic>\n                    polysaccharide (CDP) possesses antitumor, anti\u2010inflammatory, and antioxidant activity. However, the impact of CDP on osteoclasts is unclear. In this study, tartrate\u2010resistant acid phosphatase staining, immunofluorescence, reverse transcription\u2010polymerase chain reaction, and western blot analysis were utilized to demonstrate that CDP inhibited osteoclastogenesis and hydroxyapatite resorption. In addition, CDP also inhibited the expression of osteoclast maker genes including\n                    <jats:italic>Ctsk<\/jats:italic>\n                    ,\n                    <jats:italic>Mmp9<\/jats:italic>\n                    , and\n                    <jats:italic>Acp5<\/jats:italic>\n                    and had no effect on receptor activator of nuclear factor \u03baB (RANK) expression. Mechanistic analyses revealed that CDP increases the expression of antioxidant enzymes to attenuate RANKL\u2010mediated ROS production in osteoclasts and inhibits nuclear factor of activated T cells and mitogen\u2010activated protein kinase activation. These results suggest that CDP may represent a candidate drug for the treatment of osteoporosis caused by excessive osteoclast activity.\n                  <\/jats:p>","DOI":"10.1002\/jcp.26882","type":"journal-article","created":{"date-parts":[[2018,7,3]],"date-time":"2018-07-03T08:14:44Z","timestamp":1530605684000},"page":"9674-9684","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":49,"title":["<i>Cistanche deserticola<\/i>\n                    polysaccharide attenuates osteoclastogenesis and bone resorption via inhibiting RANKL signaling and reactive oxygen species production"],"prefix":"10.1002","volume":"233","author":[{"given":"Dezhi","family":"Song","sequence":"first","affiliation":[{"name":"Research Centre for Regenerative Medicine Guangxi Medical University  Nanning China"},{"name":"Guangxi Key Laboratory of Regenerative Medicine Guangxi Medical University  Nanning China"},{"name":"Department of Microbiology Guangxi 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