Dianshan Ke1, Yu Wang2, Yunlong Yu3, Yongxuan Wang4, Wang Zheng5, Xiaomin Fu6, Junyong Han7, Guoyou Zhang8, Jie Xu9. 1. Department of Orthopedics, The People's Hospital of JiangMen, Jiangmen, 529000, Guangdong, China; Academy of Orthopedics in Guangdong Province, The Third Affiliated Hospital, Southern Medical University, Guangzhou, 510630, Guangdong, China. Electronic address: kds8810@163.com. 2. Department of Orthopaedics, Chifeng Hospital, Chifeng, 024000, Inner Mongolia, China. 3. Department of Orthopedics, Fujian Provincial Hospital, Fuzhou, 350003, Fujian, China. 4. Department of Endocrine, Sanming First Hosptial, The Affiliated Sanming First Hospital of Fujian Medical University, Sanming, 365000, Fujian, China. 5. Center for Cancer and Immunology Research, Children's National Medical Center, Washington, 20010, DC, USA. 6. Division of Metabolism and Endocrinology, John Hopkins University, Baltimore, 21218, Maryland, USA. 7. Institute for Immunology, Fujian Academy of Medical Sciences, Fuzhou, 350003, Fujian, China. 8. Department of Orthopaedics, Tongliao City Hospital, Tongliao, 028000, Inner Mongolia, China. 9. Department of Orthopedics, Fujian Provincial Hospital, Fuzhou, 350003, Fujian, China. Electronic address: jiexud@126.com.
Abstract
BACKGROUND/ PURPOSE: It remains unclear what role curcumin plays in the autophagy of osteoclast precursors (OCPs) during osteoclastogenesis, since some researchers found that curcumin has the ability to inhibit osteoclastogenesis. While others have considered it as an autophagy activator. This study aimed to determine the effect of curcumin-regulated autophagy on osteoclastogenesis. RESULTS: The results revealed that direct administration of curcumin enhanced the OCP autophagy response in bone marrow-derived macrophages (BMMs). Curcumin could also abate RANKL's stimulatory effect on OCP autophagy and osteoclastogenesis. Autophagic suppression related to pharmacological inhibitors or gene silencing could further enhance the inhibitory effect of curcumin on osteoclastogenesis. As expected, curcumin ameliorated ovariectomy (OVX)-induced bone loss and its effect could be promoted by an autophagy inhibitor (chloroquine). CONCLUSIONS: In conclusion, curcumin can directly enhance the autophagic activity of OCPs, which inhibits its anti-osteoclastogeneic effects. Autophagy inhibition-based drugs are expected to enhance curcumin's efficacy in treating osteoporosis.
BACKGROUND/ PURPOSE: It remains unclear what role curcumin plays in the autophagy of osteoclast precursors (OCPs) during osteoclastogenesis, since some researchers found that curcumin has the ability to inhibit osteoclastogenesis. While others have considered it as an autophagy activator. This study aimed to determine the effect of curcumin-regulated autophagy on osteoclastogenesis. RESULTS: The results revealed that direct administration of curcumin enhanced the OCP autophagy response in bone marrow-derived macrophages (BMMs). Curcumin could also abate RANKL's stimulatory effect on OCP autophagy and osteoclastogenesis. Autophagic suppression related to pharmacological inhibitors or gene silencing could further enhance the inhibitory effect of curcumin on osteoclastogenesis. As expected, curcumin ameliorated ovariectomy (OVX)-induced bone loss and its effect could be promoted by an autophagy inhibitor (chloroquine). CONCLUSIONS: In conclusion, curcumin can directly enhance the autophagic activity of OCPs, which inhibits its anti-osteoclastogeneic effects. Autophagy inhibition-based drugs are expected to enhance curcumin's efficacy in treating osteoporosis.