Protective effects of emodin on subchondral bone and articular cartilage in osteoporotic osteoarthritis rats: A preclinical study.

BACKGROUND: Osteoporotic osteoarthritis (OP-OA) is a severe pathological form of OA, urgently requiring precise management strategies and more efficient interventions. Emodin (Emo), an effective ingredient found in the traditional Chinese medicine rhubarb, has been dEmonstrated to promote osteogenesis and inhibit extracellular matrix degradation. In this study, we aimed to investigate the interventional effects of Emo on the subchondral bone and cartilage of the knee joints in OP-OA model rats. METHODS: Thirty-two SD rats were randomly and equally divided into sham, OP-OA, Emo low-dose, and Emo high-dose groups. Micro-CT scanning was conducted to examine the bone microstructure of the rat knee joints. H&E and Safranin O and Fast Green staining (SO&FG) were performed for the pathomorphological evaluation of the rat cartilage tissues. ELISA was used to estimate the rat serum expression levels of inflammatory factors, including interleukin-1ß (IL-1ß) and tumor necrosis factor-α (TNF-α). Additionally, the CCK-8 assay was utilized for determining the viability of Emo-treated BMSCs. Western blot and real-time PCR analyses were also employed to measure the bone formation indexes and cartilage synthesis and decomposition indexes. Lastly, the osteogenic and chondrogenic differentiation efficiency of the BMSCs was investigated via Alizarin Red and Alcian Blue staining. RESULTS: Emo intervention alleviated the bone microstructural disruption of the subchondral bone and articular cartilage in the OP-OA rats and up-regulated the expression of bone and cartilage anabolic metabolism indicators, decreased the expression of cartilage catabolism indicators, and diminished the expression of inflammatory factors in the rat serum (P<0.05). Furthermore, Emo reversed the decline in the osteogenic and chondrogenic differentiation ability of the BMSCs (P<0.05). CONCLUSION: Emo intervention mitigates bone loss and cartilage damage in OP-OA rats and promotes the osteogenic and chondrogenic differentiation of BMSCs.

Total glucosides of white paeony capsule alleviate articular cartilage degeneration and aberrant subchondral bone remodeling in knee osteoarthritis.

Knee osteoarthritis (KOA) is a prevalent degenerative joint disease that is primarily managed by improving the destroyed cartilage and reversing subchondral bone remodeling. Total glucosides of white paeony (TGP) capsule primarily contains extracts from the white peony root and has been shown to have various pharmacological effects, but its role in KOA still requires comprehensive evaluation. In this study, we aimed to investigate the protective effect of TGP on knee cartilage and subchondral bone, as well as elucidate the underlying molecular mechanisms. The effect of TGP on KOA progression was evaluated in the destabilization of the medial meniscus (DMM)-induced KOA model of mouse and interleukin (IL)-1ß-induced KOA model of primary mouse chondrocytes. In vivo and in vitro experiments demonstrated that TGP had a protective effect on the cartilage. Treatment with TGP could induce the synthesis of critical elements in the cartilage extracellular matrix and downregulate the synthesis of degrading enzymes in the extracellular matrix. Regarding the underlying mechanisms, TGP inhibited the phosphorylation and nuclear translocation of p65 by regulating the nuclear factor-kappa B (NF-κB) signaling pathway. In addition, TGP could reduce the secretion of IL-1ß, IL-6, and tumor necrosis factor-α (TNF-α). Moreover, it has a sustained effect on coupled subchondral bone remodeling through regulation of the OPG/RANKL/RANK pathway. In conclusion, TGP may protect articular cartilage by downregulating the NF-κB signaling pathway and may support coupled subchondral bone remodeling by regulating OPG/RANKL/RANK signaling pathway in the DMM-induced KOA model of mouse, suggesting a new therapeutic potential for KOA treatment.