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目的探讨苯那普利对正常大鼠、阿霉素肾病大鼠尿蛋白排出量、肾功能的影响以及对系膜细胞增殖、系膜基质成分合成的作用。方法对正常及阿霉素肾病大鼠分别注射苯那普利、强的松、苯磺酸氨氯地平及生理盐水后,测定24尿蛋白排出量的变化;以自动图像分析仪测定了各组系膜细胞的定量指数、肾小球系膜基质指数;对肾组织标本进行了Ⅳ型胶原、层黏连蛋白及纤维连接蛋白的免疫组织化学染色,并以狭缝杂交法测定了层黏连蛋白的RNA转录。结果苯那普利可明显减少阿霉素肾病大鼠尿蛋白的排出量[治疗 6周(44.7± 6.0)mg/24h比治疗前(56.8 ±23.4)mg/24h],减少系膜细胞的增殖及系膜基质成分的合成。其作用与强的松组相类似,而苯磺酸氨氯地平却无此作用。结论苯那普利可直接作用于肾小球系膜基质,在转录水平抑制肾小球系膜基质的合成。
Objective To investigate the effects of benazepril on urinary albumin excretion and renal function in normal rats and adriamycin-induced nephropathy rats as well as on mesangial cell proliferation and mesangial matrix components. Methods The normal and doxorubicin nephropathy rats were injected with benazepril, prednisone, amlodipine besylate and saline, the determination of 24 urinary protein excretion changes; measured by an automatic image analyzer in each group The quantitative index of mesangial cells and glomerular mesangial matrix index were determined. Immunohistochemical staining of type Ⅳ collagen, laminin and fibronectin were performed on renal tissue samples. RNA transcription of proteins. Results Benazepril significantly reduced urinary albumin excretion in adriamycin-induced nephrotic rats (44.7 ± 6.0 mg / 24h after treatment for 6 weeks (56.8 ± 23.4) mg / 24h ], Reduce the proliferation of mesangial cells and mesangial matrix components. Its role is similar to that of prednisone, while amlodipine besylate does not. Conclusion benazapril can act directly on the glomerular mesangial matrix, inhibiting the synthesis of mesangial matrix at the transcriptional level.