检索规则说明:AND代表“并且”;OR代表“或者”;NOT代表“不包含”;(注意必须大写,运算符两边需空一格)
检 索 范 例 :范例一: (K=图书馆学 OR K=情报学) AND A=范并思 范例二:J=计算机应用与软件 AND (U=C++ OR U=Basic) NOT M=Visual
作 者:刘淑芬 王琦[2] 马亚 曾学军[4] LIU Shu-fen;WANG Qi;MA Ya;ZENG Xue-jun(Dept.of Physical Medicine & Rehabilitation,Peking Union Medical College Hospkal,CAMS & PUMC,Beijing 100730;Dept.of Rheumatology,the first Affiliated Hospital to Nanjing Medical University,Nanjing 210029;Dept.of Ultrasonic,Children' s Hospital Affiliated to Capital Institue of Pediatrics,Beijing 100020;Dept.of Genelal Internal Medicine,Peking Union Medical College Hospital,CAMS & PUMC,Beijing 100230,China)
机构地区:[1]中国医学科学院北京协和医学院北京协和医院物理医学康复科,北京100730 [2]南京医科大学第一附属医院风湿免疫科,江苏南京210029 [3]首都儿科研究所附属儿童医院超声科,北京100020 [4]中国医学科学院北京协和医学院北京协和医院普通内科,北京100730
出 处:《基础医学与临床》2018年第5期692-695,共4页Basic and Clinical Medicine
摘 要: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.
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在链接到云南高校图书馆文献保障联盟下载...
云南高校图书馆联盟文献共享服务平台 版权所有©
您的IP:216.73.216.40