ArticleScientific reports2025
Beta sitosterol inhibits the proliferation and migration of synoviocytes in rheumatoid arthritis via lactylation of GPI.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Review
- Rewiring immunity in rheumatoid arthritis: metabolic and epigenetic therapeutic strategies.Frontiers in pharmacology · 2026Review
- When metabolic enzymes meet lactylation: a bidirectional dialogue in health and disease.Frontiers in cell and developmental biology · 2026Review
- Biochemical investigations, in silico study and targeted delivery aspects of plant phytosterols: β-sitosterol.Inflammopharmacology · 2025Review
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Authors and funding
9 authors.
Funding
Abstract
Fibroblast-like synoviocytes (FLSs) are critical for promoting joint and surrounding soft tissue damage in Rheumatoid arthritis (RA). β-Sitosterol has the potential to attenuate RA; however, the underlying mechanism remains largely unknown. This study aimed to investigate the effect of β-Sitosterol on the biological functions of FLSs. FLSs were isolated from the synovial tissues of patients with RA, and cellular behaviors were evaluated using cell counting kit-8, 5-ethynyl-2'-deoxyuridine, scratch test, and enzyme-linked immunosorbent assay. The binding between β-Sitosterol and LDHA was evaluated using molecular docking and surface plasmon resonance. The lactylation of GPI was identified using immunoprecipitation (IP), western blotting, and protein stability assay. The results showed that β-Sitosterol suppressed FLS proliferation, migration, and the levels of IL-1β, IL-6, and TNF-α in a dose-dependent manner. Next, we found that β-Sitosterol bound to LDHA and decreased its protein levels. Moreover, overexpression of LDHA elevated the lactylation levels of GPI and increased GPI protein levels. Knockdown of GPI abrogated the effects on cellular behaviors induced by LDHA. In conclusion, β-Sitosterol inhibits the proliferation, migration, and inflammatory response of FLSs by suppressing LDHA-mediated lactylation of GPI, thereby attenuating RA. These findings provide insights into the molecular mechanisms of β-Sitosterol and suggest β-Sitosterol may be a therapeutic agent for RA.
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