Orcinol Glucoside Improves Senile Osteoporosis through Attenuating Oxidative Stress and Autophagy of Osteoclast via Activating Nrf2/Keap1 and mTOR Signaling Pathway

Figure 9

A schematic diagram illustrating the potential mechanism of orcinol glucoside (OG)’s effects in a mouse model of senile osteoporosis. OG inhibited osteoclastogenesis by scavenging ROS, subsequently elevating the expression of antioxidant enzymes via activating the Nrf2/Keap1 pathway and inhibiting autophagy by activating the mTOR pathway. Thus, OG is a promising candidate drug for the treatment of bone disorders related with aging and oxidative stress, especially senile osteoporosis in the future.