Betulinic Acid Inhibits RANKL-Induced Osteoclastogenesis via Attenuating Akt, NF-κB, and PLCγ2-Ca<sup>2+</sup> Signaling and Prevents Inflammatory Bone Loss
Da Hye Jeong, Sung Chul Kwak, Myeung Su Lee, Kwon‐Ha Yoon, Ju‐Young Kim, Chang Hoon Lee
Abstract
influx. BA also significantly inhibited the expression of osteoclastogenesis-specific marker genes. Moreover, we found that BA administration restored the bone loss induced through acute lipopolysaccharide injection in mice by a micro-CT and histological analysis. Our findings suggest that BA is a potential therapeutic candidate for bone diseases involving osteoclasts.
Topics & Concepts
OsteoclastBone resorptionRANKLBetulinic acidBone remodelingChemistryProtein kinase BNF-κBCancer researchSignal transductionPharmacologyCell biologyEndocrinologyBiochemistryActivator (genetics)MedicineBiologyReceptorGeneticsBone Metabolism and DiseasesNatural product bioactivities and synthesisNF-κB Signaling Pathways