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Updated: Jul 3, 2025
Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
Published on: March 18, 2022
α-Solanine attenuates chondrocyte pyroptosis to improve osteoarthritis via suppressing NF-κB pathway
Jinyi Zhou1,2, Jinting Wu1,3, Fangda Fu1
1Institute of Orthopaedics and Traumatology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Traditional Chinese Medicine), Hangzhou, China.
Abstract:
α-Solanine has been shown to exhibit anti-inflammatory and anti-tumour properties; however, its efficacy in treating osteoarthritis (OA) remains ambiguous. The study aimed to evaluate the therapeutic effects of α-solanine on OA development in a mouse OA model. The OA mice were subjected to varying concentrations of α-solanine, and various assessments were implemented to assess OA progression. We found that α-solanine significantly reduced osteophyte formation, subchondral sclerosis and OARSI score. And it decreased proteoglycan loss and calcification in articular cartilage. Specifically, α-solanine inhibited extracellular matrix degradation by downregulating collagen 10, matrix metalloproteinase 3 and 13, and upregulating collagen 2. Importantly, α-solanine reversed chondrocyte pyroptosis phenotype in articular cartilage of OA mice by inhibiting the elevated expressions of Caspase-1, Gsdmd and IL-1β, while also mitigating aberrant angiogenesis and sensory innervation in subchondral bone. Mechanistically, α-solanine notably hindered the early stages of OA progression by reducing I-κB phosphorylation and nuclear translocation of p65, thereby inactivating NF-κB signalling. Our findings demonstrate the capability of α-solanine to disrupt chondrocyte pyroptosis and sensory innervation, thereby improving osteoarthritic pathological progress by inhibiting NF-κB signalling. These results suggest that α-solanine could serve as a promising therapeutic agent for OA treatment.
Insights
Alpha-solanine effectively treats osteoarthritis (OA) by reducing joint damage and inflammation. This natural compound inhibits chondrocyte pyroptosis and NF-κB signaling, offering a promising therapeutic approach for OA.
Area of Science:
- Pharmacology
- Rheumatology
- Molecular Biology
Background:
- Osteoarthritis (OA) is a degenerative joint disease with limited treatment options.
- Alpha-solanine possesses known anti-inflammatory and anti-tumor properties, but its role in OA is unclear.
Purpose of the Study:
- To investigate the therapeutic potential of alpha-solanine in a mouse model of osteoarthritis.
- To elucidate the molecular mechanisms underlying alpha-solanine's effects on OA progression.
Main Methods:
- Administration of varying concentrations of alpha-solanine to mice with induced OA.
- Assessment of OA progression through histological analysis (osteophyte formation, proteoglycan loss, OARSI score).
- Evaluation of molecular markers related to extracellular matrix degradation, chondrocyte pyroptosis, angiogenesis, innervation, and NF-κB signaling.
Main Results:
- Alpha-solanine significantly reduced osteophyte formation, subchondral sclerosis, and proteoglycan loss.
- It inhibited extracellular matrix degradation and reversed chondrocyte pyroptosis by modulating Caspase-1, Gsdmd, and IL-1β.
- Alpha-solanine mitigated aberrant angiogenesis and sensory innervation, and inactivated NF-κB signaling by inhibiting I-κB phosphorylation and p65 translocation.
Conclusions:
- Alpha-solanine demonstrates significant therapeutic effects in an OA mouse model.
- It improves OA pathology by inhibiting chondrocyte pyroptosis and sensory innervation via the NF-κB pathway.
- Alpha-solanine represents a potential novel therapeutic agent for osteoarthritis treatment.
