Gordon T P, Clifton P, James M J, Roberts-Thomson P J
Ann Rheum Dis. 1986 Aug;45(8):673-6. doi: 10.1136/ard.45.8.673.
The effect of coating monosodium urate crystals (MSU) with low density lipoprotein (LDL), postulated previously as a major regulator of gouty inflammation, was studied in a neutrophil chemiluminescence (CL) assay and an air pouch model of inflammation induced by MSU. LDL crystalline coating abrogated the neutrophil CL response but, in contrast, had no inhibitory effect on leucocyte accumulation, levels of the prostaglandin (PG) metabolite 6-keto-PGF1 alpha, and exudation of plasma proteins in the in vivo model. This latter observation raises doubts about the postulated physiological role of LDL in terminating the acute gouty attack.
低密度脂蛋白(LDL)包裹尿酸单钠晶体(MSU)的作用,此前被假定为痛风性炎症的主要调节因子,在中性粒细胞化学发光(CL)试验和MSU诱导的炎症气袋模型中进行了研究。LDL晶体包裹消除了中性粒细胞的CL反应,但与之相反,在体内模型中,对白细胞积聚、前列腺素(PG)代谢物6-酮-PGF1α水平和血浆蛋白渗出没有抑制作用。后一观察结果对LDL在终止急性痛风发作中假定的生理作用提出了质疑。