A Novel RANKL-Targeted Furoquinoline Alkaloid Ameliorates Bone Loss in Ovariectomized Osteoporosis through Inhibiting the NF-κB Signal Pathway and Reducing Reactive Oxygen Species

Figure 8

The process and mechanism by which DIC can inhibit osteoclast formation. Schematic diagram of the molecular regulation of DIC RANKL-induced osteoclastogenesis. DIC leads to attenuation of nuclear translocation and autoamplification of NFATc1 through inhibition of RANKL and RANK binding, MAPK and NF-κB pathways, and blockade of calcium oscillations. The production of reactive oxygen species (ROS) and scavenging of ROS by antioxidant enzymes are regulated by DIC. GTP: guanosine-5-triphosphate; MAPK: mitogen-activated protein kinase; JNK: c-Jun N-terminal kinase; TRAF6: TNF receptor-associated factor 6; Erk: extracellular signal-regulated kinase; NFATc1: nuclear factor 1 of activated T cells.