It also blocked RANKL-induced activation of osteoclastogenic signals including ERK and p38 and the expression of nuclear factor of activated T cells cytoplasmic 1, as a master regulator of osteoclast differentiation, leading to decreased expression of osteoclast-specific marker genes such as Atp6v0d2, DC-STAMP and cathepsin K. Micro-computed tomography revealed that a seven-week oral administration of BLE0 dramatically improved ovariectomy-induced trabecular bone loss.
Together, CA ameliorated osteoclast formation and CIA-induced bone loss in db/db mice through inflammation suppression by regulating ROS-dependent p38 pathway.