ArticleJournal of cellular and molecular medicine2022
Sparstolonin B suppresses free fatty acid palmitate-induced chondrocyte inflammation and mitigates post-traumatic arthritis in obese mice.
Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Immunometabolic reprogramming in osteoporosis-osteoarthritis comorbidity: from inflammaging to osteochondral unit degeneration.Frontiers in immunology · 2026Review
- Lung-targeting lipid nanoparticle-mediated sparstolonin B delivery improves acute lung injury.Biomaterials science · 2025Article
- The Toll-like Receptor-2/4 Antagonist, Sparstolonin B, and Inflammatory Diseases: A Literature Mining and Network Analysis.Cardiovascular drugs and therapy · 2025Article
- Targeting mTOR with curcumin: therapeutic implications for complex diseases.Inflammopharmacology · 2025Review
- Effect of plasma free fatty acids on lung function in male COPD patients.Scientific reports · 2025Article
- Exploration of the association between estimated glucose disposal rate and osteoarthritis in middle-aged and older adults: An analysis of NHANES data from 2011 to 2018.Open medicine (Warsaw, Poland) · 2025Article
- Fatty acid metabolism in gouty arthritis: mechanisms to therapeutic targeting.Frontiers in immunology · 2025Review
- Sparstolonin B nano-formulation attenuates LPS-induced lung injury.Frontiers in pharmacology · 2025Article
- Regulating lipid metabolism in osteoarthritis: a complex area with important future therapeutic potential.Annals of medicine · 2024Review
- Beyond mechanical loading: The metabolic contribution of obesity in osteoarthritis unveils novel therapeutic targets.Heliyon · 2023Review
- Sparstolonin B suppresses free fatty acid palmitate-induced chondrocyte inflammation and mitigates post-traumatic arthritis in obese mice.Journal of cellular and molecular medicine · 2022Article
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11 authors at 1 institution in 1 country.
Funding
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Abstract
Abnormal lipid metabolism, such as systemic increased free fatty acid, results in overproduction of pro-inflammatory enzymes and cytokines, which is crucial in the development of obesity-related osteoarthritis (OA). However, there are only a few drugs that target the lipotoxicity of OA. Recent researches have documented that the traditional Chinese medicine, Sparstolonin B (Ssn B), exerted anti-inflammatory effects in various diseases, but not yet in OA. On the basis of this evidence, our works purposed to evaluate the effect of Ssn B on free fatty acid (FFA) palmitate (PA)-stimulated human osteoarthritic chondrocytes and obesity-associated mouse OA model. We found that Ssn B suppressed PA-triggered inflammatory response and extracellular matrix catabolism in a concentration-dependent approach. In vivo, Ssn B treatment inhibited cartilage degeneration and subchondral bone calcification caused by joint mechanical imbalance and alleviated metabolic inflammation in obesity. Mechanistically, co-immunoprecipitine and molecular docking analysis showed that the formation of toll-like receptor 4 (TLR4)/myeloid differentiation protein-2 (MD-2) complex caused by PA was blocked by Ssn B. Subsequently, it leads to inactivation of PA-caused myeloid differentiation factor 88 (MyD88)-dependent nuclear factor-kappaB (NF-κB) cascade. Together, these findings demonstrated that Ssn B is a potential treatment agent for joint degenerative diseases in obese individuals.
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