Aucubin alleviates knee osteoarthritis in mice by suppressing the NF‑κB signaling pathway.
10.12122/j.issn.1673-4254.2025.10.06
- Author:
Yongxin MAI
1
;
Shuting ZHOU
2
;
Ruijia WEN
2
;
Jinfang ZHANG
1
;
Dongxiang ZHAN
2
Author Information
1. Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen 518000, China.
2. Guangdong Engineering Technology Research Center of Commercialization of Lingnan Special Medical Institution Preparations, Guangzhou 510405, China.
- Publication Type:Journal Article
- Keywords:
aucubin;
cartilage repair;
matrix metalloproteinases;
nuclear factor-κB;
osteoarthritis
- MeSH:
Animals;
Mice, Inbred C57BL;
Mice;
Osteoarthritis, Knee/drug therapy*;
Signal Transduction/drug effects*;
NF-kappa B/metabolism*;
Iridoid Glucosides/therapeutic use*;
SOX9 Transcription Factor/metabolism*;
Chondrocytes/drug effects*;
Male;
Interleukin-1beta/metabolism*;
Matrix Metalloproteinase 13/metabolism*;
Collagen Type II/metabolism*;
Disease Models, Animal
- From:
Journal of Southern Medical University
2025;45(10):2104-2110
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVES:To assess the therapeutic effect of aucubin in mice with knee osteoarthritis (KOA) and investigate the underlying mechanism.
METHODS:Sixty C57BL/6J mice were randomized equally into sham operation group, KOA model group, glucosamine (positive control) treatment group, and low-, medium-, and high-dose aucubin treatment groups (2, 4, and 8 mg/kg, respectively). KOA mouse models were established by transection of the anterior cruciate ligament (ACL), and the treatment was initiated on day 1 postoperatively and administered weekly for 8 weeks. Safranin O-fast green staining, immunohistochemistry, and microCT were used to evaluate the changes in cartilage pathology, inflammatory protein expression, and subchondral bone volume fraction (BV/TV). The expression levesl of COL2, SOX9, p-P65, IL-1β and MMP13 proteins in the cartilage tissues were detected using Western blotting. In a chondrocyte model with IL-1β treatment for mimicking KOA, the effect of aucubin on chondrogenic differentiation was observed with Alcian blue and Safranin O staining, and cellular COL2, SOX9 and TNF‑α mRNA expressions were detected with RT-qPCR.
RESULTS:Compared with those in the model group, the mouse models receiving aucubin treatment showed significantly upregulated COL2 and SOX9 protein levels and downregulated p-P65, IL-1β and MMP13 expressions in the cartilage tissues. In the IL-1β-induced chondrocyte model, aucubin treatment significantly upregulated the mRNA expressions of SOX9 and COL2 but lowered the mRNA expression of TNF-α. Alcian blue and Safranin O staining confirmed that aucubin promoted the synthesis of cartilage extracellular matrix and enhanced chondrogenic differentiation of the cells.
CONCLUSIONS:Aucubin can effectively alleviate KOA in mice by inhibiting NF‑κB-mediated cartilage inflammation, promoting cartilage matrix synthesis, and improving subchondral bone microstructure.
