泊那司他（司他立）抑制醛糖还原酶并不能预防长期糖尿病大鼠的蛋白尿。
Aldose reductase inhibition by ponalrestat (statil) does not prevent proteinuria in long-term diabetic rats.
作者信息
Reddi A S, Jyothirmayi G N
机构信息
Department of Medicine, UMDN New Jersey Medical School, Newark 07103.
出版信息
J Diabetes Complications. 1993 Oct-Dec;7(4):233-40.
The aldose reductase pathway has been implicated in the development of chronic complications of diabetes. In this study, we investigated the effect of an aldose reductase inhibitor, statil, on glomerular synthesis of heparan sulfate and albuminuria in male Wistar rats made diabetic with streptozotocin. Heparan sulfate is the predominant glycosaminoglycan (GAG) proteoglycan in the glomerular basement membrane (GBM). It confers a negative charge on the GBM, and its loss has been related to the presence of albumin in the urine. Diabetic rats synthesized less glomerular heparan sulfate and excreted more albumin than normal rats. Glomerular sorbitol concentration was significantly higher in diabetic than in normal rats. Chronic treatment of diabetic rats with statil did not improve either heparan sulfate synthesis or albuminuria despite normalization of glomerular sorbitol content. The present study does not support the role of excess sorbitol in the development of glomerular abnormalities in this rat model of streptozotocin diabetes.
醛糖还原酶途径与糖尿病慢性并发症的发生发展有关。在本研究中，我们调查了醛糖还原酶抑制剂斯塔蒂尔对用链脲佐菌素诱导糖尿病的雄性Wistar大鼠肾小球硫酸乙酰肝素合成及蛋白尿的影响。硫酸乙酰肝素是肾小球基底膜（GBM）中主要的糖胺聚糖（GAG）蛋白聚糖。它赋予GBM负电荷，其丢失与尿中白蛋白的存在有关。糖尿病大鼠肾小球硫酸乙酰肝素合成减少，白蛋白排泄量比正常大鼠多。糖尿病大鼠肾小球山梨醇浓度显著高于正常大鼠。尽管肾小球山梨醇含量恢复正常，但用斯塔蒂尔对糖尿病大鼠进行长期治疗并未改善硫酸乙酰肝素合成或蛋白尿。本研究不支持过量山梨醇在链脲佐菌素糖尿病大鼠模型肾小球异常发生发展中的作用。
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