Instituto de Ciências da Atividade Física e Esportes, Universidade Cruzeiro do Sul, São Paulo, Brazil.
Clin Exp Immunol. 2011 Mar;163(3):362-7. doi: 10.1111/j.1365-2249.2010.04300.x. Epub 2010 Dec 22.
Serum amyloid A (SAA) levels are elevated highly in acute phase response and elevated slightly and persistently in chronic diseases such as rheumatoid arthritis and diabetes. Given that fibroblasts exert profound effects on progression of inflammatory chronic diseases, the aim of this study was to investigate the response of fibroblasts to SAA. A dose-dependent increase in O(2) (-) levels was observed by treatment of fibroblasts with SAA (r = 0·99 and P ≤ 0·001). In addition, the expression of p47-phox was up-regulated by SAA (P < 0·001) and diphenyliodonium (DPI), a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, reduced the release of O(2) (-) by 50%. Also, SAA raised fibroblast proliferation (P < 0·001) and this effect was completely abolished by the addition of anti-oxidants (P < 0·001). These findings support the notion that, in chronic inflammatory sites, SAA activated fibroblast proliferation and ROS production.
血清淀粉样蛋白 A(SAA)在急性期反应中显著升高,在类风湿关节炎和糖尿病等慢性疾病中轻度持续升高。鉴于成纤维细胞对炎症性慢性疾病的进展有深远影响,本研究旨在研究 SAA 对成纤维细胞的反应。用 SAA(r = 0.99 和 P ≤ 0.001)处理成纤维细胞,观察到 O2(-)水平呈剂量依赖性增加。此外,SAA(P < 0.001)上调 p47-phox 的表达,烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶抑制剂二苯基碘(DPI)使 O2(-)的释放减少 50%。此外,SAA 增加成纤维细胞增殖(P < 0.001),而添加抗氧化剂可完全消除该作用(P < 0.001)。这些发现支持这样一种观点,即在慢性炎症部位,SAA 激活成纤维细胞增殖和 ROS 产生。