109906
论文已发表
注册即可获取德孚的最新动态
IF 收录期刊
- 3.4 Breast Cancer (Dove Med Press)
- 3.2 Clin Epidemiol
- 2.6 Cancer Manag Res
- 2.9 Infect Drug Resist
- 3.7 Clin Interv Aging
- 5.1 Drug Des Dev Ther
- 3.1 Int J Chronic Obstr
- 6.6 Int J Nanomed
- 2.6 Int J Women's Health
- 2.9 Neuropsych Dis Treat
- 2.8 OncoTargets Ther
- 2.0 Patient Prefer Adher
- 2.2 Ther Clin Risk Manag
- 2.5 J Pain Res
- 3.0 Diabet Metab Synd Ob
- 3.2 Psychol Res Behav Ma
- 3.4 Nat Sci Sleep
- 1.8 Pharmgenomics Pers Med
- 2.0 Risk Manag Healthc Policy
- 4.1 J Inflamm Res
- 2.0 Int J Gen Med
- 3.4 J Hepatocell Carcinoma
- 3.0 J Asthma Allergy
- 2.2 Clin Cosmet Investig Dermatol
- 2.4 J Multidiscip Healthc
已发表论文
黄芪甲苷通过 p53/SLC7A11/GPX4 轴抑制软骨细胞铁死亡从而缓解骨关节炎
Authors Tang Z, Cheng L , Li M , Chen J , Huang C
Received 8 October 2025
Accepted for publication 14 November 2025
Published 19 November 2025 Volume 2025:18 Pages 16169—16186
DOI https://doi.org/10.2147/JIR.S572167
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Ujjwol Risal
Zhongfu Tang,1,* Lili Cheng,1,* Ming Li,1 Junjie Chen,2 Chuanbing Huang1
1Department of Rheumatology, The First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, Anhui, 230031, People’s Republic of China; 2College of Traditional Chinese Medicine, Anhui University of Chinese Medicine, Hefei, Anhui, 230012, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Chuanbing Huang, Department of Rheumatology, The First Affiliated Hospital of Anhui University of Chinese Medicine, No. 117 Meishan Road, Shushan District, Hefei, Anhui, People’s Republic of China, Email chuanbingh@ahtcm.edu.cn
Purpose: Osteoarthritis (OA) is a chronic joint disease characterized by articular cartilage damage. Astragaloside IV (AS-IV), a cyclic triterpenoid saponin extracted from Astragalus membranaceus, exhibits antioxidant and cartilage-protective activities. However, its mechanism of action in OA remains unclear. To study the efficacy and mechanism of action of AS-IV in the treatment of OA.
Methods: In the SW1353 cell model treated with IL-1β, cell viability was detected by CCK-8, and the ultrastructure of mitochondria was observed by transmission electron microscopy. Multiple methods such as flow cytometry, immunofluorescence, Western blotting, and fluorescent probe method were used to evaluate the effects of AS-IV on chondrocyte ferroptosis and extracellular matrix degradation, and the results were verified by rescue experiments. An OA rat model was established, and multiple methods such as histopathology were used to evaluate the therapeutic effect of AS-IV on OA cartilage injury.
Results: In vitro experiments have shown that IL-1β can induce ferroptosis in chondrocytes. Overexpression of p53 promotes ferroptosis in chondrocytes and exacerbates the progression of OA. AS-IV can downregulate the expression of p53 and MMP13, while upregulating the expression of SLC7A11, GPX4, SOX9, Col II, and GSH. Additionally, AS-IV reduces intracellular levels of ROS, MDA, and Fe2+. In an OA rat model, AS-IV significantly reduces the Osteoarthritis Research Society International (OARSI) score and Mankin score, alleviating cartilage damage. Furthermore, AS-IV inhibits extracellular matrix degradation and lipid peroxidation in cartilage tissue.
Conclusion: AS-IV inhibits chondrocyte ferroptosis by modulating the p53/SLC7A11/GPX4 axis, thereby alleviating cartilage damage and OA. This suggests that AS-IV has therapeutic potential for OA treatment.
Keywords: osteoarthritis, astragaloside IV, chondrocytes, ferroptosis, lipid peroxidation
1Department of Rheumatology, The First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, Anhui, 230031, People’s Republic of China; 2College of Traditional Chinese Medicine, Anhui University of Chinese Medicine, Hefei, Anhui, 230012, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Chuanbing Huang, Department of Rheumatology, The First Affiliated Hospital of Anhui University of Chinese Medicine, No. 117 Meishan Road, Shushan District, Hefei, Anhui, People’s Republic of China, Email chuanbingh@ahtcm.edu.cn
Purpose: Osteoarthritis (OA) is a chronic joint disease characterized by articular cartilage damage. Astragaloside IV (AS-IV), a cyclic triterpenoid saponin extracted from Astragalus membranaceus, exhibits antioxidant and cartilage-protective activities. However, its mechanism of action in OA remains unclear. To study the efficacy and mechanism of action of AS-IV in the treatment of OA.
Methods: In the SW1353 cell model treated with IL-1β, cell viability was detected by CCK-8, and the ultrastructure of mitochondria was observed by transmission electron microscopy. Multiple methods such as flow cytometry, immunofluorescence, Western blotting, and fluorescent probe method were used to evaluate the effects of AS-IV on chondrocyte ferroptosis and extracellular matrix degradation, and the results were verified by rescue experiments. An OA rat model was established, and multiple methods such as histopathology were used to evaluate the therapeutic effect of AS-IV on OA cartilage injury.
Results: In vitro experiments have shown that IL-1β can induce ferroptosis in chondrocytes. Overexpression of p53 promotes ferroptosis in chondrocytes and exacerbates the progression of OA. AS-IV can downregulate the expression of p53 and MMP13, while upregulating the expression of SLC7A11, GPX4, SOX9, Col II, and GSH. Additionally, AS-IV reduces intracellular levels of ROS, MDA, and Fe2+. In an OA rat model, AS-IV significantly reduces the Osteoarthritis Research Society International (OARSI) score and Mankin score, alleviating cartilage damage. Furthermore, AS-IV inhibits extracellular matrix degradation and lipid peroxidation in cartilage tissue.
Conclusion: AS-IV inhibits chondrocyte ferroptosis by modulating the p53/SLC7A11/GPX4 axis, thereby alleviating cartilage damage and OA. This suggests that AS-IV has therapeutic potential for OA treatment.
Keywords: osteoarthritis, astragaloside IV, chondrocytes, ferroptosis, lipid peroxidation