Cryptotanshinone inhibits RANKL-induced osteoclastogenesis by regulating ERK and NF-κB signaling pathways.

Abstract

Osteoporosis (OS) is one of the most common healthy problems characterized by low bone mass. Osteoclast, the primary bone-resorbing cell, is responsible for destructive bone diseases including osteoporosis (OS). Cryptotanshinone (CTS), an active component extracted from the root of Salvia miltiorrhiza bunge, has been shown to prevent the destruction of cartilage and the thickening of subchondral bone in mice osteoarthritis models. However, its molecular mechanism in osteoclastogenesis needs to be determined. The aim of the current study was to explore the effect of CTS on osteoclastogenesis and further evaluate the underlying mechanism. Our results showed that CTS inhibited receptor activator of NF-κB ligand (RANKL)-induced the increase in tartrate-resistant acid phosphatase (TRAP) activity in bone marrow-derived macrophages (BMMs). In addition, the expressions of osteoclastogenesis-related marker proteins and nuclear factor of activated T-cells (NFAT) activation were suppressed by CTS treatment in BMMs. Furthermore, CTS attenuated RANKL-induced ERK phosphorylation and NF-κB activation in BMMs. These findings indicated that CTS inhibited RANKL-induced osteoclastogenesis by inhibiting ERK phosphorylation and NF-κB activation in BMMs. Thus, CTS may function as an inhibitor of osteoclastogenesis and may be considered as an alternative medicine for the prevention and treatment of OS.