Anti-inflammatory and Antioxidant Effect of Poly-gallic Acid (PGAL) in an In Vitro Model of Synovitis Induced by Monosodium Urate Crystals

Gout is a chronic and degenerative disease that affects the joints and soft tissues because of the crystalline deposit of monosodium urate. The interaction between monosodium urate crystals (MSU) and synoviocytes generates oxidative and inflammatory states. These physiological characteristics have promoted the study of poly-gallic acid (PGAL), a poly-oxidized form of gallic acid reported to be effective in in vitro models of inflammation. The effect of PGAL in an in vitro model of oxidation and synovial inflammation induced by MSU was evaluated after 24 h of stimulation through the morphological changes, the determination of oxidative stress (OS), IL-1 beta and the phagocytosis of the MSU. A 20% reduction in synovial viability and the generation of vesicles were observed when they were exposed to MSU. When PGAL was used at 100 and 200 mu g/ml, cell death was reduced by 30% and 17%, respectively. PGAL both doses reduce the vesicles generated by MSU. OS generation in synoviocytes exposed to 100 mu g/ml and 200 mu g/ml PGAL decreased by 1.28 and 1.46 arbitrary fluorescence units (AFU), respectively, compared to the OS in synoviocytes exposed to MSU (1.9 AFU). PGAL at 200 mu g/ml inhibited IL-1 beta by 100%, while PGAL at 100 mu g/ml inhibited IL-1 beta by 66%. The intracellular MSU decreased in synoviocytes stimulated with 100 mg/ml PGAL. The PGAL has a cytoprotective effect against damage caused by MSU in synoviocytes and can counteract the oxidative and inflammatory response induced by the crystals probably because it exerts actions at the membrane level that prevent phagocytosis of the crystals.

Automated summary

This study evaluated the effect of poly-gallic acid (PGAL) in an in vitro model of oxidation and synovial inflammation induced by monosodium urate (MSU) crystals. The results showed that PGAL reduced cell death and vesicle generation, decreased oxidative stress, and inhibited the inflammatory response. PGAL exhibited a cytoprotective effect against MSU-induced damage in synoviocytes.