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Updated: Jun 4, 2025
Standardized Histomorphometric Evaluation of Osteoarthritis in a Surgical Mouse Model
Published on: May 6, 2020
Andrographolide suppresses fibrogenic phenotype of chondrocytes and ameliorates osteoarthritis by regulating
Yaoyu Xiang1, Xidan Hu2, Xianguang Yang1
1Department of Sports Medicine, First Affiliated Hospital of Kunming Medical University, Kunming, 650000, Yunnan, China.
Background:
Pathogenic degeneration of cartilage and the generation of fibrotic cartilage are crucial characteristics linked to the progression of osteoarthritis (OA). The current research aims to explore the potential function of the miR-137/BMP7 pathway in regulating the fibrogenic transition of chondrocytes associated with OA, as well as assess the therapeutic potential of andrographolide.
Methods:
Samples of cartilage from the knees of patients with OA and individuals without OA were gathered to investigate the expression patterns of miR-137, BMP7, and markers associated with fibrosis. A cell model using primary chondrocytes stimulated with interleukin (IL)-1β was developed to study the involvement of the miR-137/BMP7 axis during the fibrogenic transition of these cells. Additionally, we utilized an animal model of OA in order to assess the beneficial effects of the anti-inflammatory natural compound andrographolide on the fibrogenesis induced by OA in vivo.
Results:
Elevated levels of fibrogenic and inflammatory factors were linked to decreased miR-137 expression in OA samples. In IL-1β-treated chondrocytes, there was an upregulation of fibrogenic markers alongside a reduction in miR-137 levels. The overexpression of miR-137 inhibited fibrogenesis through the negative regulation of BMP7. Additionally, treatment with andrographolide was effective in attenuating the fibrogenic phenotype in chondrocytes and mitigating OA pathogenesis via modulating the miR-137/BMP7 pathway.
Conclusion:
miR-137 downregulation and BMP7 overexpression might contribute to the fibrogenic features in OA-related chondrocytes. Andrographolide attenuates fibrogenic phenotype in chondrocytes and alleviates the severity of OA by modulating the miR-137/BMP7 axis.
Insights
MicroRNA-137 (miR-137) downregulation and increased Bone Morphogenetic Protein 7 (BMP7) contribute to osteoarthritis (OA) fibrogenesis. Andrographolide treatment alleviates OA by modulating the miR-137/BMP7 pathway.
Area of Science:
- Biomedical research
- Molecular biology
- Osteoarthritis research
Background:
- Osteoarthritis (OA) is characterized by cartilage degeneration and fibrotic cartilage formation.
- The miR-137/BMP7 pathway's role in chondrocyte fibrogenic transition in OA is not fully understood.
Purpose of the Study:
- To investigate the function of the miR-137/BMP7 pathway in OA chondrocyte fibrogenesis.
- To evaluate andrographolide's therapeutic potential in OA.
Main Methods:
- Cartilage samples from OA patients and controls were analyzed for miR-137, BMP7, and fibrosis markers.
- A cell model of OA using IL-1β-stimulated primary chondrocytes was established.
- An OA animal model was used to assess andrographolide's effects.
Main Results:
- OA samples showed decreased miR-137 and increased fibrogenic/inflammatory factors.
- IL-1β-induced chondrocytes exhibited reduced miR-137 and increased fibrogenesis.
- miR-137 overexpression inhibited fibrogenesis by downregulating BMP7.
- Andrographolide treatment reduced chondrocyte fibrogenesis and OA severity.
Conclusions:
- Downregulation of miR-137 and overexpression of BMP7 contribute to OA chondrocyte fibrogenesis.
- Andrographolide alleviates OA by modulating the miR-137/BMP7 axis, reducing the fibrogenic phenotype.
