Rheumatology
Can gastrodin calm RA by blocking histone lactylation?
Open access · cc by · source: Europe PMC
Gastrodin bound KAT8 (KD 413.72 μM), lowered H3K9la, cut IL-6/MMP signals in FLS and THP-1 cells, and eased joint swelling in AIA rats at 20 mg/kg.
Study at a glance
- Design
- Animal / in-vitro — LPS-stimulated FLS/THP-1 cultures plus Sprague-Dawley rat adjuvant-induced arthritis; docking/SPR targeting KAT8
- N
- N=5 · AIA rats randomly grouped n=5 per group (AIA, GAS, DEX); plus in vitro FLS and THP-1 macrophage assays
- Population
- Rheumatoid-arthritis models: fibroblast-like synoviocytes, THP-1 macrophages, and SD rat AIA
- Outcome
- Inflammatory cytokines/MMPs, H3K9 lactylation, KAT8 stability, and joint swelling/synovial hyperplasia
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Key findings
GAS inhibited IL-6, MMP1, and MMP13 via lower glycolysis/lactate. SPR KD was 413.72 μM. GAS destabilized KAT8 and reduced H3K9la. In AIA rats, 20 mg/kg lessened swelling and synovial hyperplasia with lower H3K9la and IL-6.
Methodology
Treated LPS-stimulated FLS and THP-1 macrophages with gastrodin (10–20 μM), confirmed KAT8 binding by docking and SPR, manipulated KAT8, and tested 20 mg/kg gastrodin in Sprague-Dawley AIA rats.
Limitations
Cell and rat AIA data do not equal a human RA trial; micromolar SPR affinity is modest, so clinical dosing and safety are unproven.
How this study connects
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