Gentiopicroside inhibits RANKL-induced osteoclastogenesis by regulating NF-κB and JNK signaling pathways

• Published in: Biomedicine & pharmacotherapy Vol. 100; pp. 142 - 146
• Main Authors: Chen, Fangqing, Xie, Lin, Kang, Ran, Deng, Rongrong, Xi, Zhipeng, Sun, Daoxi, Zhu, Jin, Wang, Liming
• Format: Journal Article
• Language: English
• Published: France Elsevier Masson SAS 01.04.2018
• Subjects: Gentiopicroside; JNK pathway; NF-κB pathway; Osteoporosis; RANKL; JNK pathway; Osteoporosis; RANKL; NF-κB pathway; Gentiopicroside
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2018.02.014

[Display omitted] Gentiopicroside, a main active component from the traditional Chinese herb medicine Gentiana manshurica Kitag, has been shown to possess anti-arthritis effect. However, the molecular mechanism of gentiopicroside on the osteoclast formation remains unclear. The present study was designed to investigate the effects and mechanisms of gentiopicroside on receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis. The results showed that pre-treatment with gentiopicroside significantly inhibited RANKL-induced osteoclast formation from mouse bone marrow macrophages (BMMs). In addition, we observed that gentiopicroside efficiently suppressed osteoclastogenesis-related marker genes expression in RANKL-stimulated BMMs. Mechanistically, gentiopicroside suppressed RANKL-induced the activation of JNK and NF-κB signaling pathways in BMMs. Taken together, the present study demonstrated that gentiopicroside inhibits RANKL-induced osteoclastogenesis through the inactivation of JNK and NF-κB signaling pathways. Thus, gentiopicroside may be a promising agent for the treatment of osteoporosis.