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2023, Vol. 27 ›› Issue (26): 4113-4119

Astragaloside IV can reduce interleukin-1beta-induced chondrocyte inflammation

Huang Shaoshuo1, Li Jiacheng1, Luo Di2, Zhu Kai1, Xu Bo2, Xue Yuanliang1, Yan Bozhao1, Li Gang1   

  1. 1The First Clinical Medical College of Shandong University of Traditional Chinese Medicine, Jinan 250014, Shandong Province, China; 2The Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250014, Shandong Province, China

  • Received:2022-04-27 Accepted:2022-06-29 Online:2023-09-18 Published:2023-01-20

  • Contact: Li Gang, MD, Professor, Chief physician, The First Clinical Medical College of Shandong University of Traditional Chinese Medicine, Jinan 250014, Shandong Province, China

  • About author:Huang Shaoshuo, Master candidate, The First Clinical Medical College of Shandong University of Traditional Chinese Medicine, Jinan 250014, Shandong Province, China

  • Supported by:

    the National Natural Science Foundation of China, No. 82074453 (to LG); Shandong Medical and Health Science and Technology Development Project, No. 202004071045 (to XB)


Abstract: BACKGROUND: Osteoarthritis is one of the most common degenerative diseases, and there are still no drugs to delay or reverse the disease. Only anti-inflammatory and analgetic treatments can be performed to relieve symptoms and improve patient’s conditions in the short term. Astragaloside IV is an active component of Astragalus membranaceus with immunomodulatory, ischemic protection, cardiac protection, anti-inflammatory, antiviral, and anti-tumor effects.  
OBJECTIVE: To investigate the effects of astragaloside IV on interleukin-1β-induced ATDC5 cell injury and its related mechanism.  
METHODS: ATDC5 cells were randomly divided into blank control group, model group, monomer group, and experimental group. There was no intervention in the blank control group. Cells in the latter three groups were treated with 100 μg/L interleukin-1β, 5 μg/L astragaloside IV, and 100 μg/L interleukin-1β+5 μg/L astragaloside IV, respectively. After 18 hours of treatment, cell counting kit-8 was used to detect cell proliferation. Western blot and qRT-PCR were used to detect the expression of matrix metalloproteinases 3, 9, 13, type II collagen, stromal cell-derived factor 1 (SDF-1), and C-X-C chemokine receptor 4 (CXCR4) at protein and mRNA levels, respectively. Toluidine blue staining was used to detect cell morphological changes and cell numbers, and trypan blue staining was used to detect cell viability.
RESULTS AND CONCLUSION: Interleukin-1β (100 μg/L) significantly inhibited the activity of ATDC5 cells, increased the expression of inflammatory markers (matrix metalloproteinases 3, 9, and 13), decreased the expression of type II collagen, increased the expression of SDF-1 and CXCR4, activated the SDF-1/CXCR4 pathway, and induced inflammatory responses in cells. Compared with the model group, astragaloside IV significantly reduced the expression of matrix metalloproteinases 3, 9, and 13, and increased the expression of type II collagen, indicating that astragaloside IV can alleviate chondrocyte injury induced by interleukin-1β. In addition, the expression of CXCR4 and SDF-1 was decreased in the experimental group compared with the model group, indicating that astragaloside IV alleviates interleukin-1β-induced chondrocyte inflammation through the SDF-1/CXCR4 signaling pathway.  

Key words: osteoarthritis, astragaloside IV, SDF-1/CXCR4 signaling pathway, ATDC5 cell, inflammatory response


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