Crider J Y, Yorio T, Sharif N A, Griffin B W
Molecular Pharmacology Unit, Alcon Laboratories, Inc., Fort Worth, Texas, USA.
J Ocul Pharmacol Ther. 1997 Aug;13(4):337-52. doi: 10.1089/jop.1997.13.337.
The effects of stimulated hyperglycemia on the Na+/K(+)-ATPase activity of cultured bovine retinal pigment epithelial (RPE) cells were investigated. Total Rb+ uptake, measured by a chromatographic method, was decreased 20-30% by 55.5 mM glucose relative to 5.55 mM glucose for culture periods of 2 to 28 days. An acute hyperglycemic stress (< 1 week) had no effect on ouabain-inhibition of Rb+ uptake or ouabain binding to RPE cells (IC50 = 55 nM for both processes) and did not alter the IC50 value (near 10 nM) for binding of strophanthidin, another selective Na+/K(+)-ATPase inhibitor. A small increase in the apparent K(m) of Rb+ for Na+/K(+)-ATPase accompanied the decrease in maximal Rb+ uptake at 55.5 mM glucose. The continuous presence of AL-1576, an aldose reductase inhibitor (ARI), normalized the effect of severe hyperglycemia on Rb+ uptake in the chronic (28 days) but not the acute exposure protocols. Thus, decreased efficiency of Na+/K(+)-ATPase caused by chronic accumulation of intracellular sorbitol can account for previously reported functional and structural alterations in the RPE cell layer of diabetic rodents. The results of the present study suggest that hyperglycemia-induced loss of Na+/K(+)-ATPase function in RPE cells, which responds to aldose reductase inhibitor treatment, contributes to the pathogenesis of diabetic retinopathy.
研究了刺激的高血糖对培养的牛视网膜色素上皮(RPE)细胞Na+/K(+)-ATP酶活性的影响。通过色谱法测量的总铷摄取量,在5.55 mM葡萄糖条件下培养2至28天时,相对于55.5 mM葡萄糖,降低了20%-30%。急性高血糖应激(<1周)对哇巴因抑制铷摄取或哇巴因与RPE细胞结合没有影响(两个过程的IC50均为55 nM),并且没有改变毒毛旋花子苷(另一种选择性Na+/K(+)-ATP酶抑制剂)结合的IC50值(接近10 nM)。在55.5 mM葡萄糖条件下,Na+/K(+)-ATP酶对铷的表观米氏常数(Km)略有增加,同时最大铷摄取量下降。醛糖还原酶抑制剂(ARI)AL-1576的持续存在,使严重高血糖对慢性(28天)而非急性暴露方案中铷摄取的影响恢复正常。因此,细胞内山梨醇的慢性积累导致的Na+/K(+)-ATP酶效率降低,可以解释先前报道的糖尿病啮齿动物RPE细胞层的功能和结构改变。本研究结果表明,高血糖诱导的RPE细胞中Na+/K(+)-ATP酶功能丧失,对醛糖还原酶抑制剂治疗有反应,这有助于糖尿病视网膜病变的发病机制。