Laboratorio de Líquido Sinovial, Instituto Nacional de Rehabilitación "Luis Guillermo Ibarra Ibarra", Ciudad de Mexico, México.
Unidad de Ingeniería de Tejidos Terapia Celular Y Medicina Regenerativa, Instituto Nacional de Rehabilitación "Luis Guillermo Ibarra Ibarra", Ciudad de Mexico, México.
Inflammation. 2022 Oct;45(5):2066-2077. doi: 10.1007/s10753-022-01676-3. Epub 2022 May 3.
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-1β, 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 µg/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 µg/ml and 200 µg/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 µg/ml inhibited IL-1β by 100%, while PGAL at 100 µg/ml inhibited IL-1β by 66%. The intracellular MSU decreased in synoviocytes stimulated with 100 µg/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.
痛风是一种慢性退行性疾病，由于单钠尿酸盐晶体的沉积而影响关节和软组织。单钠尿酸盐晶体（MSU）与滑膜细胞的相互作用产生氧化和炎症状态。这些生理特征促进了多没食子酸（PGAL）的研究，PGAL 是一种报道在炎症的体外模型中有效的没食子酸的多氧化形式。通过形态变化、氧化应激（OS）、IL-1β的测定以及 MSU 的吞噬作用，评估了 PGAL 在由 MSU 诱导的体外氧化和滑膜炎症模型中的作用。当它们暴露于 MSU 时，滑膜活力降低 20%，并且观察到囊泡形成。当使用 100 和 200μg/ml 的 PGAL 时，细胞死亡分别减少了 30%和 17%。两种剂量的 PGAL 均可减少 MSU 产生的囊泡。与暴露于 MSU 的滑膜细胞中的 OS（1.9 AFU）相比，暴露于 100μg/ml 和 200μg/ml PGAL 的滑膜细胞中的 OS 生成分别降低了 1.28 和 1.46 个任意荧光单位（AFU）。PGAL 在 200μg/ml 时抑制了 100%的 IL-1β，而 PGAL 在 100μg/ml 时抑制了 66%的 IL-1β。用 100μg/ml PGAL 刺激的滑膜细胞中细胞内 MSU 减少。PGAL 对 MSU 引起的滑膜细胞损伤具有细胞保护作用，并且可以对抗晶体诱导的氧化和炎症反应，可能是因为它在膜水平上发挥作用，从而阻止晶体的吞噬作用。
