长期单纯高尿酸血症大鼠主动脉病理变化

Pathological changes of arota in long-term pure hyperuricemia rat

目的探索长期单纯高尿酸血症(HU)能否造成大鼠主动脉的病理变化。方法将大鼠随机分为对照组和HU模型组,模型组使用2%的氧嗪酸钾饲料和100μmol/L的尿酸水饲养,后期增加氧嗪酸钾灌胃建立长期HU动物模型,使用HE染色观察大鼠主动脉内膜-中膜厚度、内皮炎性细胞浸润以及脂纹、脂斑的形成,使用免疫组化检测大鼠主动脉e NOS、ET-1、ICAM的表达,使用ELISA检测ET-1、ICAM的含量、酶法检测血清NO含量。结果 HU组大鼠可见动脉壁内膜-中膜厚度轻度增加;浸润于内膜的炎性细胞数轻度增多。HU组主动脉内膜e NOS表达较对照组明显减少,ET-1、ICAM表达显著高于对照组(P<0.05),HU组大鼠血清ET-1(P<0.05)、ICAM(P<0.01)均较对照组显著升高,NO(P<0.01)较对照组显著降低。结论长期单纯高尿酸血症(12周)可以造成S-D大鼠主动脉早期内皮损伤,但不能形成典型动脉粥样硬化。

Objective To identify whether long-term hyperuricemia（ HU） is able to induce arota pathological changes in rat. Methods 2% OA forage and 100 μmol/L uric acid plus OA lavage were used to copy a long-term hyperuricemia animal model,e NOS,ET-1,ICAM expression in arota was evaluated to find out the role of uric acid in cardiovascular diseases. Results The arotas of hyperuricemia rats had tiny damages whereas that of rats in control group was totally normal; Hyperuricemia rat had less e NOS expression,more ET-1,ICAM expression in arota（ P〈0. 05） and less NO,more ET-1,ICAM in serum.Conclusions Long-term hyperuricemia is able to induce impairment in endothelium in rat arota,but fails to cause atherosclerosis.