Fernández-Rodríguez Jennifer A, Almonte-Becerril Maylin, Ramil-Gómez Olalla, Hermida-Carballo Laura, Viñas-Diz Susana, Vela-Anero Ángela, Concha Ángel, Camacho-Encina María, Blanco Francisco J, López-Armada María J
Grupo de Investigación en Envejecimiento e Inflamación, SERGAS, Complexo Hospitalario Universitario A Coruña (CHUAC), Instituto de Investigación Biomédica A Coruña (INIBIC), Agrupación Estratégica CICA-INIBIC, As Xubias 84, A Coruña, 15006, Spain.
Universidad Intercultural Estado de Puebla, Calle Principal a Lipuntahuaca S/N, Lipuntahuaca, Puebla, 73475, México.
Mol Nutr Food Res. 2021 Jan;65(2):e2000377. doi: 10.1002/mnfr.202000377. Epub 2020 Dec 7.
Previous work reported that dietary supplementation with resveratrol lowers synovial hyperplasia, inflammatory and oxidative damage in an antigen-induced arthritis (AIA) model. Here, it is investigated whether resveratrol can regulate the abnormal synovial proliferation by inducing autophagy and controlling the associated inflammatory response.
Animals treated with resveratrol 8 weeks before AIA induction show the highest significant signal for microtubule-associated protein 1 light chain 3 by confocal microscopy. Besides, resveratrol significantly reduces p62 expression, but it does not increase the signal of beclin-1. Also, active caspase-3 expression, as well as poly(ADP-ribose) polymerase, is upregulated in the AIA group, and is significantly reduced in resveratrol-treated AIA group. Resveratrol also mitigates angiopoietin-1 and vascular endothelial growth factor signals. Finally, resveratrol significantly reduces the serum levels of IL-1β, C reactive protein, and prostaglandin E2, as well as nuclear factor κB synovial tissue expression, which shows a significant correlation with p62 expression.
Dietary supplementation with resveratrol induces the noncanonical autophagy pathway and limits the cross-talk with inflammation, which in consequence modulates the synovial hyperplasia. Preventive strategies that incorporate dietary intervention with resveratrol may offer a potential therapeutic alternative to drugs to influence the risk of rheumatoid arthritis and influence its course.
先前的研究报道，在抗原诱导的关节炎（AIA）模型中，补充白藜芦醇饮食可降低滑膜增生、炎症和氧化损伤。在此，研究白藜芦醇是否可通过诱导自噬和控制相关炎症反应来调节异常的滑膜增殖。
在诱导AIA前8周用白藜芦醇治疗的动物，通过共聚焦显微镜观察显示微管相关蛋白1轻链3的信号最强。此外，白藜芦醇显著降低p62表达，但不增加beclin-1的信号。此外，AIA组中活性半胱天冬酶-3表达以及聚（ADP-核糖）聚合酶上调，而在白藜芦醇治疗的AIA组中显著降低。白藜芦醇还可减轻血管生成素-1和血管内皮生长因子信号。最后，白藜芦醇显著降低血清白细胞介素-1β、C反应蛋白和前列腺素E2水平，以及核因子κB滑膜组织表达，其与p62表达呈显著相关性。
补充白藜芦醇饮食可诱导非经典自噬途径并限制与炎症的相互作用，从而调节滑膜增生。将饮食干预与白藜芦醇相结合的预防策略可能为药物提供一种潜在的治疗选择，以影响类风湿性关节炎的风险并影响其病程。
