Fuscoside Attenuates Bone Loss in Bone Defects by Regulating The Rankl/Nlrp3/Opg Pathway in Rats

(Pages: 451-456)
Xiangwei Liu, M.D., Binfeng Wang, M.D., *
Department of Traumatic Orthopedics, Chifeng Municipal Hospital, Chifeng, Inner Mongolia, China
Department of Traumatic Orthopedics, Chifeng Municipal Hospital, Chifeng, Inner Mongolia, China
*Corresponding Address: Department of Traumatic Orthopedics Chifeng Municipal Hospital Chifeng Inner Mongolia China Email:wangbinfeng1258@qq.com
The Cell Journal (Yakhteh) is an open access journal which means the articles are freely available online for any individual author to download and use the providing address. The journal is licensed under a Creative Commons Attribution-Non Commercial 3.0 Unported License which allows the author(s) to hold the copyright without restrictions that is permitting unrestricted use, distribution, and reproduction in any medium provided the original work is properly cited. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Liu Xiangwei, Wang Binfeng. Fuscoside Attenuates Bone Loss in Bone Defects by Regulating The Rankl/Nlrp3/Opg Pathway in Rats. Cell J. 2021; 23(4): 451-456.

Abstract

Objective

This study evaluated the beneficial effect of fuscoside in the repair of bone defects (BDs) and the possible molecular mechanism thereof.

Materials and Methods

In this experimental study, a BD was induced by drilling the rat tibia. The rats were then administered oral fuscoside, at 200 or 300 mg/kg, for 2 weeks. The effect of treatment was assessed based on the bone formation score and on the levels of cytokines and biochemical markers in serum. Tibial expression of the proteins involved in the Rankl/Nlrp3/Opg pathway was determined by quantitative reverse-transcription polymerase chain reaction and western blot assay, and histopathological changes by haematoxylin and eosin and TRAP staining.

Results

In the fuscoside-treated BD rats, the bone formation score improved and inflammatory cytokine levels were reduced. The levels of biochemical markers improved as well, as did the expression of apoptosis proteins. Fuscoside also attenuated the expression of Rankl, Opg, Nlrp3, Runx2, Osterix, and Osteocalcin (Oc) proteins in the tibial tissue of the BD rats and reversed the abnormal histopathological changes.

Conclusion

These results suggest that fuscoside improves BD repair by reducing the differentiation of osteoclasts and by regulating the Rankl/Nlrp3/Opg pathway.