摘要
目的:观察基质金属蛋白酶 9(matrixmetalloprotei nase 9,MMP 9)及组织金属蛋白酶抑制剂 1(tissueinhibitorof metalloproteinase 1,TIMP 1)在阿霉素肾病大鼠肾小管中的表 达变化.方法:采用大鼠尾静脉单剂量注射阿霉素7.5mg/kg 建立阿霉素肾病模型,免疫组织化学检测正常对照组、阿霉素 肾病组肾组织MMP 9及TIMP 1的表达变化;光镜下观察肾 小管间质形态学改变;尿液标本检测尿N 乙酰 βD氨基葡萄 糖苷酶(N acetyl beta D glucosaminidase,NAG),β2 微球蛋白 (β2 microglobulin,β2 MG),24h尿蛋白量的变化.结果:阿 霉素肾病组大鼠肾小管间质损害明显,24h尿蛋白定量增多, 尿β2 MG及尿NAG酶活力升高;肾小管上皮细胞MMP 9的 表达明显上调(P<0.05),于第14日达高峰.肾小管的TIMP 1的表达上调,第14,28,56日与同期对照组相比差异显著 (P<0.05).结论:阿霉素肾病大鼠肾小管上皮细胞MMP 9, TIMP 1表达异常可能参与肾小管病变的发生发展过程.
AIM: To investigate the expression features of MMP-9 and TIMP-1 in renal tubulointerstitial tissues in rats with adriamycin-induced nephropathy and their significance. METHODS: The mice model of nephropathy was established by tail vein injection of adriamycin 7.5 mg/kg. The renal histopathological changes, the urine protein excretion, urinary NAG and β2-MG were examined. The expressions of MMP-9 and TIMP-1 in the cortex of the kidneys were examined by immunohistochemistry. RESULTS: The tubulointerstitial injury, the excretion of urine protein, urinary NAG and β2-MG in nephrotic rats significantly increased as compared with those of the normal control group. In nephropathy group, the expression of MMP-9 in the tubular cells increased on day 7 and reached the peak on day 14, with significantly higher quantities than those in normal group(P<0.05). The expression of TIMP-1 increased significantly compared with that in the normal group on day 14, day 28 and day 56(P<0.05). CONCLUSION: The abnormal expression of MMP-9 and TIMP-1 in the tubular cells contributes to the pathogenesis of tubulointerstitial fibrosis.
出处
《第四军医大学学报》
北大核心
2005年第5期407-410,共4页
Journal of the Fourth Military Medical University
关键词
基质金属蛋白酶
组织金属蛋白酶抑制剂
肾小管
纤维化
matrix metalloproteinases
tissue inhibitor of metalloproteinase
kidney tubules
fibrosis
