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Cinnamaldehyde attenuates streptozocin-induced diabetic osteoporosis in a rat model by modulating netrin-1/DCC-UNC5B signal transduction.
Ji, Songjie; Zhao, Bingjia; Gao, Yuan; Xie, Jun; Han, Huijun; Wu, Qunli; Yang, Dan.
Afiliación
  • Ji S; Department of Orthopaedic Surgery, Beijing Jishuitan Hospital, Capital Medical University, Beijing, China.
  • Zhao B; Department of Joint Surgery, Beijing Jishuitan Guizhou Hospital, Guiyang, China.
  • Gao Y; Department of Traditional Chinese Medicine, Peking Union Medical College Hospital, Peking Union Medical College, Translational Medicine Center, Chinese Academy of Medical Sciences, Beijing, China.
  • Xie J; Department of Joint Surgery, Beijing Jishuitan Guizhou Hospital, Guiyang, China.
  • Han H; Department of Traditional Chinese Medicine, Peking Union Medical College Hospital, Peking Union Medical College, Translational Medicine Center, Chinese Academy of Medical Sciences, Beijing, China.
  • Wu Q; Department of Epidemiology and Biostatistics, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and School of Basic Medicine, Peking Union Medical College, Beijing, China.
  • Yang D; Department of Traditional Chinese Medicine, Peking Union Medical College Hospital, Peking Union Medical College, Translational Medicine Center, Chinese Academy of Medical Sciences, Beijing, China.
Front Pharmacol ; 15: 1367806, 2024.
Article en En | MEDLINE | ID: mdl-38628640
ABSTRACT

Background:

Cinnamaldehyde (CMD) is a major functional component of Cinnamomum verum and has shown treatment effects against diverse bone diseases. This study aimed to assess the anti-diabetic osteoporosis (DOP) potential of diabetes mellitus (DM) and to explore the underlying mechanism driving the activity of CMD.

Methods:

A DOP model was induced via an intraperitoneal injection of streptozocin (STZ) into Sprague-Dawley rats, and then two different doses of CMD were administered to the rats. The effects of CMD on the strength, remodeling activity, and histological structure of the bones were assessed. Changes in the netrin-1 related pathways also were detected to elucidate the mechanism of the anti-DOP activity by CMD.

Results:

CMD had no significant effect on the body weight or blood glucose level of the model rats. However, the data showed that CMD improved the bone strength and bone remodeling activity as well as attenuating the bone structure destruction in the DOP rats in a dose-dependent manner. The expression of netrin-1, DCC, UNC5B, RANKL, and OPG was suppressed, while the expression of TGF-ß1, cathepsin K, TRAP, and RANK was induced by the STZ injection. CMD administration restored the expression of all of these indicators at both the mRNA and protein levels, indicating that the osteoclast activity was inhibited by CMD.

Conclusion:

The current study demonstrated that CMD effectively attenuated bone impairments associated with DM in a STZ-induced DOP rat model, and the anti-DOP effects of CMD were associated with the modulation of netrin-1/DCC/UNC5B signal transduction.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Front Pharmacol Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Suiza
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Front Pharmacol Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Suiza