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- Title
水飞蓟宾调控 TLR4/NF-κB 通路介导的细胞凋亡改善膝骨性关节炎模型大鼠软骨损伤.
- Authors
徐天波; 刘德国; 张颉鸿; 吕骜; 侯振海
- Abstract
Objective To investigate the effect of silybinin (SB) on cartilage injury in a rat model of knee osteoarthritis (KOA) and explore its impact on the Toll-like receptor 4 (TLR4) /nuclear factor-κB (NF-κB) pathway and cell apoptosis.Methods SD rats were divided into a normal control group, model group, and SB group, with 8 rats in each group (total n=24) .The KOA model was established by intra-articular injection of papain, followed by 6 weeks of SB intervention.Histological changes were observed using safranin O-fast green and hematoxylin-eosin staining, and histological scoring was performed using the Osteoarthritis Research Society International (OARSI) scoring system.Western blot was used to detect the expression changes of TLR4, NF-κB, p65, BAX, BCL-2, and Caspase-3 proteins.Results The OARSI score of the knee joint cartilage tissue in the model group was significantly higher than that in the normal control group (P <0.000 1) .Additionally, the levels of TLR4, NF-κB, p65, BAX, and Caspase3 proteins in the subchondral bone tissue of the model group were significantly increased, while the expression level of the anti-apoptotic protein BCL-2 was significantly decreased (P <0.000 1) .Compared with the model group, the OARSI score of the joint cartilage tissue in the SB group was significantly lower (P <0.001), and the expression levels of TLR4, NF-κB, p65, BAX, and Caspase3 proteins in the subchondral bone tissue were significantly down-regulated, while the expression level of BCL-2 was significantly upregulated (P <0.000 1) .Conclusion Silybinin inhibits cell apoptosis by suppressing the activation of the TLR4/NF-κB pathway in subchondral bone, thereby repairing cartilage injury in the rat model of KOA.
- Publication
Guangdong Medical Journal, 2024, Vol 45, Issue 5, p560
- ISSN
1001-9448
- Publication type
Article
- DOI
10.13820/j.cnki.gdyx.20232950