Abstract：Objective: To explore the osteoprotective effect of curcumin on osteoarthritis (OA) model rats based on the ferroptosis pathway. Methods: Chondrocytes were isolated and cultured from 6-8-week-old SD rats.The cells were divided into the control group,the model group (LPS group),the extremely low-dose curcumin group (1μmoL/L),the low-dose curcumin group (10μmoL/L),the medium-dose curcumin group (20μmoL/L),the high-dose curcumin group (40μmoL/L),and the ferroptosis inhibitor ferrostatin-1 (Fer-1) group.Except for the control group,primary chondrocytes in all other groups were treated with lipopolysaccharide (LPS) to establish OA cell models.Cells in the curcumin groups were treated with corresponding doses of curcumin,while cells in the Fer-1 group were treated with 1μM Fer-1.After 48 hours,cell morphology and damage were observed using toluidine blue staining.Cell apoptosis was detected using the TUNEL method.Cell viability was assessed using the CCK-8 assay.The levels of reactive oxygen species (ROS) and malondialdehyde (MDA) were measured using reagent kits.Western blot (WB) was used to detect the protein expression of acyl-CoA synthetase long-chain family member 4 (ACSL4) and glutathione peroxidase 4 (GPX4).Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure the mRNA expression levels of GPX4,heat shock protein B1 (HSPB1),and telomere repeat binding factor 1 (TRF1). Results: Compared with the control group,the LPS group showed a reduced number of chondrocytes,damaged cell morphology,smaller cell nuclei,increased apoptosis rate,elevated levels of MDA and ROS,upregulated ACSL4 protein and TRF1 mRNA expression,and decreased cell viability,GPX4 protein,and GPX4 and HSPB1 mRNA expression (P<0.001).Compared with the LPS group,the low-dose,medium-dose,and high-dose curcumin groups and the Fer-1 group exhibited improved chondrocyte injury,reduced apoptosis rate,restored cell viability,decreased levels of MDA,ROS,ACSL4 protein,and TRF1 mRNA expression,and increased GPX4 protein and GPX4 and HSPB1 mRNA expression (P<0.05). Conclusion: Curcumin can effectively reverse LPS-induced damage to OA chondrocytes.The mechanism may be related to improving cellular antioxidant activity,regulating the expression of ferroptosis-related genes (ACSL4,GPX4,HSPB1,and TRF1),and inhibiting chondrocyte ferroptosis.
李杨, 路坦, 庄全魁, 王海涛, 陈勇, 白亮, 李伟. 基于铁死亡途径探究姜黄素对骨关节炎模型大鼠的骨保护作用[J]. 河北医学, 2025, 31(4): 591-597.
LI Yang, LU Tan, et al. Exploring the Osteoprotective Effect of Curcumin on Osteoarthritis Model Rats Based on the Ferroptosis Pathway. HeBei Med, 2025, 31(4): 591-597.
2025, Vol. 31 
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