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Published on: June 2, 2023
Anemonin attenuates osteoarthritis progression through inhibiting the activation of IL-1β/NF-κB pathway
Zuqiang Wang1, Junlan Huang1, Siru Zhou1
1Department of Rehabilitation Medicine, Center of Bone Metabolism and Repair, State Key Laboratory of Trauma, Burns and Combined Injury, Trauma Center, Research Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing, China.
Abstract:
The osteoarthritis (OA) progression is now considered to be related to inflammation. Anemonin (ANE) is a small natural molecule extracted from various kinds of Chinese traditional herbs and has been shown to inhibiting inflammation response. In this study, we examined whether ANE could attenuate the progression of OA via suppression of IL-1β/NF-κB pathway activation. Destabilization of the medial meniscus (DMM) was performed in 10-week-old male C57BL/6J mice. ANE was then intra-articularly injected into joint capsule for 8 and 12 weeks. Human articular chondrocytes and cartilage explants challenged with interleukin-1β (IL-1β) were treated with ANE. We found that ANE delayed articular cartilage degeneration in vitro and in vivo. In particular, proteoglycan loss and chondrocyte hypertrophy were significantly decreased in ANE -treated mice compared with vehicle-treated mice. ANE decreased the expressions of matrix metalloproteinase-13 (MMP13), A disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5), collagen X (Col X) while increasing Aggrecan level in murine with DMM surgery. ANE treatment also attenuated proteoglycan loss in human cartilage explants treated with IL-1β ex vivo. ANE is a potent protective molecule for OA; it delays OA progression by suppressing ECM loss and chondrocyte hypertrophy partially by suppressing IL-1β/NF-κB pathway activation.
Insights
Anemonin (ANE) effectively delays osteoarthritis progression by inhibiting inflammation and protecting cartilage. This natural compound reduces key markers of cartilage degeneration and chondrocyte hypertrophy in both animal models and human explants.
Area of Science:
- Biochemistry
- Pharmacology
- Orthopedics
Background:
- Osteoarthritis (OA) progression is increasingly linked to inflammatory processes.
- Anemonin (ANE), a natural molecule from traditional herbs, exhibits anti-inflammatory properties.
- The IL-1β/NF-κB pathway is implicated in OA pathogenesis.
Purpose of the Study:
- To investigate the potential of Anemonin (ANE) in attenuating osteoarthritis (OA) progression.
- To determine if ANE suppresses the IL-1β/NF-κB pathway activation in OA.
- To evaluate the protective effects of ANE on articular cartilage in vitro and in vivo.
Main Methods:
- Osteoarthritis was induced in mice using destabilization of the medial meniscus (DMM) surgery.
- Anemonin (ANE) was administered intra-articularly to mice over 8 and 12 weeks.
- Human articular chondrocytes and cartilage explants were challenged with interleukin-1β (IL-1β) and treated with ANE.
Main Results:
- ANE treatment significantly delayed articular cartilage degeneration in both in vitro and in vivo models.
- Proteoglycan loss and chondrocyte hypertrophy were notably reduced in ANE-treated mice.
- ANE decreased the expression of MMP13, ADAMTS5, and Collagen X, while increasing Aggrecan levels.
- ANE attenuated proteoglycan loss in human cartilage explants challenged with IL-1β.
Conclusions:
- Anemonin (ANE) demonstrates potent protective effects against osteoarthritis progression.
- ANE delays OA by suppressing extracellular matrix (ECM) loss and chondrocyte hypertrophy.
- ANE's mechanism involves partial suppression of the IL-1β/NF-κB pathway activation.
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