Sinensetin serves as an AMPK activator to inhibit RANKL-induced osteoclastogenesis via osteoclast cytoskeleton reorganization.

ABSTRACT: Osteoporosis is a skeletal condition caused by an excess of osteoclasts, resulting in an imbalance in bone metabolism. Sinensetin (SIN), one of the main ingredients in citrus fruits, provides a variety of pharmacological properties, like antioxidant, but its effects on osteoporosis remains unknown. Herein, we explored at how SIN affected RANKL-induced osteoclastogenesis and ovariectomy (OVX)-induced osteoporotic mice. Our research found that SIN, without compromising cell viability, inhibited RANKL-mediated osteoclastogenesis and the NFATc1 signaling pathway in a concentration-dependent manner. Further, RNA sequencing analysis suggested that the molecular mechanism of SIN inhibitory effect on osteoclasts is related to the cytoskeleton reorganization. The results indicated that SIN prevents

SUBMITTER: Gao Y 

PROVIDER: S-EPMC12275404 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature