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作 者:郭丽琴[1,2] 陶静莉[1] 李尚妹[1] 梁东[1] 唐德燊[1] 陈孝文[1] 刘华锋[1]
机构地区:[1]广东医学院附属医院肾病研究所,广东湛江524001 [2]山西省长治医学院附属医院肾内科,长治046000
出 处:《中国临床药理学杂志》2010年第4期292-295,共4页The Chinese Journal of Clinical Pharmacology
基 金:广东省自然科学基金资助项目(7009939);广东省科技计划基金资助项目(2008B030301022)
摘 要:目的观察罗格列酮(胰岛素增敏药)对阿霉素致肾病大鼠的尿蛋白排泌量及肾小球蛋白表达的影响。方法用罗格列酮治疗阿霉素诱导的局灶节段性肾小球硬化(FSGS)大鼠模型;用双缩脲法动态检测大鼠24h尿蛋白量;分别用荧光实时定量PCR和免疫组织化学法检测大鼠肾组织synaptopodin mRNA和蛋白表达量。结果罗格列酮能显著减缓FSGS大鼠尿蛋白排泄量的增加(P<0.05);恢复大鼠肾组织蛋白表达量(P<0.05),而不影响其mRNA表达量(P>0.05);FSGS大鼠肾组织蛋白表达量与尿蛋白排泄量呈负相关(P<0.01)。结论罗格列酮能减轻FSGS模型尿蛋白排泌量,其机制可能部分与维持足细胞足突肌动蛋白微丝骨架系统的稳定有关。Objective To investigate the effects of rosiglitazone and its possible mechanism on urinary protein excretion in adriamycin -induced nephropathy rat models. Methods Rosiglitazone therapy was performed on Focal segmental glomerulosclerosis (FSGS) rat model induced by intravenous injection with adriamycin. 24 - hour urine protein exctetion was assessed dynamically by biuret method. The mRNA and protein expression of synaptopodin in renal cortex of each group were assayed by real - time quantitative PCR and immunohistochemistry after animals were sacririced. Results Urinary protein excretion increasing was retarded by the treatment of rosiglitazone. Rosiglitazone treatment also partially restored the staining of synaptopodin (P 〈 0. 05 ) but not affect its mRNA expression ( P 〉 0. 05 ). Furthermore, synaptopodin expression was positively correlated with the urinary protein excretion. Conclusion Rosiglitazone can reduce urinary protein excretion in FSGS and its mechamism may partly relate to glomeruli synaptopodin expression up -regulaion.
关 键 词:罗格列酮 局灶节段性肾小球硬化症大鼠模型 尿蛋白排泌量 肾小球硬化
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