鹌鹑高尿酸血症模型发病机理研究

Pathogenesis of hyperuricacidemia in quail model

目的选择与尿酸、脂代谢密切相关的酶学指标,通过观察不同病理阶段高尿酸血症鹌鹑各种酶活性变化,探讨该模型可能的发病机理。方法采用生化及分子生物学方法,动态观察血清及组织中黄嘌呤氧化酶(XO)、鸟嘌呤脱氨酶(GD)、腺苷脱氨酶(ADA)、脂蛋白酯酶(LPL)、肝脂酶(HL)的活性及基因表达情况。结果模型组动物肝脏XO活性升高,基因表达显著增强,GD活性变化不明显,ADA及LPL活性显著降低,HL活性呈更迭变化。结论鹌鹑高尿酸血症模型的病理机制可能与肝XO活性升高、LPL活性降低有关;ADA、HL活性变化与高尿酸血症病理进程之间的关系有待进一步探讨。

Objective To investigate the pathogenesis of hyperuricacidemia in quail model by observing the changes of various kinds of enzyme activity in different pathological stages. Methods Biochemical and molecular biological methods were applied to dynamically observe activity and gene expression of xanthine oxidase （XO） , Guanosine deaminase （GD） , adenosine deaminase （ADA） , lipoproteinesterase （LPL） and hepatic lipoidase （HL） in serum and tissue. Results In the model group, XO activity and gene expression in the liver increased, while ADA and LPL activity decreaced significantly. GD activity had no significant change and HL activity changed alternatively. Conclusion The pathogenesis of hyperuricacidemia in quail model may be associated with increased XO activity and reduced LPL activity. The relationship between the activity of ADA and HL and pathological process of hyperuricacidemia needs to be further investigated.