Related Experiment Video
Updated: Jul 8, 2025

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
Published on: March 18, 2022
Curculigoside inhibits osteoarthritis via the regulation of NLRP3 pathway
Xufei Wang1, Yinlian Liu2, Yongnian Zhou3
1Department of Clinical Laboratory, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan; Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan. 546675488@qq.com.
Abstract:
Osteoarthritis (OA) is characterized by degenerative articular cartilage. Nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) plays an important role in inflammation. This study aims to investigate whether protective effects of curculigoside on OA are medicated by the regulation of NLRP3 pathway. Destabilization of the medial meniscus (DMM) was performed to build an OA mouse model. After surgery, OA mice were treated with curculigoside. Immunohistochemistry was conducted to evaluate OA cartilage. In addition, human chondrocytes were isolated and treated with curculigoside. The mRNA and protein expression of iNOS, MMP-9, NLRP3 was detected by PCR and Western blot analysis. Curculigoside inhibited mRNA and protein levels of iNOS and MMP-9 induced by DMM surgery in a dose-dependent manner. Furthermore, the expression of NLRP3, NF-κB and PKR was downregulated after curculigoside administration. Moreover, curculigoside reversed the effects of IL-1β on MMP-9, iNOS and type II collagen expression at mRNA and protein levels in human chondrocytes in a dose-dependent manner. In conclusion, curculigoside exhibits beneficial effect on cartilage via the inhibition of NLRP3 pathway.
More Related Videos
Related Concept Videos
NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The...
The JAK-STAT Signaling Pathway
Hedgehog Signaling Pathway
Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids

