The effects of chitosan oligosaccharides on OPG and RANKL expression in a rat osteoarthritis model

Abstract

Purpose: To investigate the effect of chitosan oligosaccharides (COS) against osteoarthritis (OA) and preliminarily discuss the osteoprotegerin (OPG), receptor activator of NF-κB ligand (RANKL) and RANK expression in a rat OA model. Methods: Thirty-six 6-week-old Male SD rats were randomly divided into three groups: shamoperated group(CON), OA-induction group(OA), COS intervention group(n=12/group). At 4 weeks after the operation, COS (50 ul) intervention weekily for consecutive 5 weeks. The OA and CON groups received an injection of 50 ul physiological saline. At death, 11 weeks following surgery, cartilage was harvested and total RNA and protein were extracted. Both the morphological changes of the cartilage were observed and harvested the total RNA and protein.Meanwhile, the expression of OPG, RANKL and RANK in cartilage were determined. Results: The expression of OPG and RANKL were both enhanced in the cartilage of the OA model. Compared with the OA group, COS treatment improved the cartilage damage (both extent and grade). Furthermore, the COS group showed highly OPG and lower RANKL. Simultaneously, COS treatment upregulated the ratio of OPG/RANKL and downregulated the RANKL/RANK. Conclusion: Chitosan oligosaccharides may be used as a unique biological agent to prevent and treat osteoarthritis, and this effect is associated with modulation of the expression of osteoprotegerin and receptor activator of NF-κB ligand.

Modulation of bone turnover aberration: A target for management of primary osteoporosis in experimental rat model

“…Treatment of osteoporotic rats with nCh/HA caused a significant down-regulation in RANKL gene expression level when compared to the untreated osteoporotic rats. This finding is comparable with that obtained by Zhang et al [125] who reported that in chitosan oligosaccharide-treated osteoarthritis-induced rats, RANKL secretion is inhibited while OPG is enhanced, RANKL/OPG mRNA ratio is significantly decreased, and RNAKL/RANK mRNA ratio is decreased. ROS raises the count of osteoclasts and induces resorption in vitro and in vivo by provoking RANKL and TNF-α expression via NF-кB [126,127].…”

Chitosan oligosaccharides packaged into rat adipose mesenchymal stem cells-derived extracellular vesicles facilitating cartilage injury repair and alleviating osteoarthritis

“…In this study, COS was packaged into rat AMSC-derived EVs, and the effects of EVs-COS on cartilage injury repair both in vitro and in vivo were explored. Previous studies have suggested that MSC-derived EVs can attenuate OA [ 30 ], and that COS can improve cartilage damage, thus, preventing and treating OA [ 31 ]. Our research found that EVs-COS could enhance the viability and migration of chondrocytes induced by IL-1β and suppress their apoptosis.…”

The emerging role of fibroblast‐like synoviocytes‐mediated synovitis in osteoarthritis: An update

“…Owing to its anti‐apoptotic and chondro‐protective characteristics, achieved via regulating the p38 MAPK signalling pathway, COS has been demonstrated to have potential as a OA treatment 108 . Moreover, COS increased the expression of osteoprotegerin (OPG) and decreased the expression of receptor activator of the NF‐κB ligand (RANKL) 109 . In addition to its protective effect on cartilage, COS was also shown to have powerful anti‐inflammatory effects by activating AMPK and extenuating inflammatory responses in OA‐FLS.…”