Restoration of nitric oxide production by aldose reductase inhibitor in human endothelial cells cultured in high-glucose medium

被引：9

作者：

Okuda, Y ^{[1
]}

Kawashima, K ^{[1
]}

Suzuki, S ^{[1
]}

Asakura, Y ^{[1
]}

Asano, M ^{[1
]}

Tsurumaru, K ^{[1
]}

Dai, HQ ^{[1
]}

Tachi, Y ^{[1
]}

Bannai, C ^{[1
]}

Saitoh, M ^{[1
]}

Yamashita, K ^{[1
]}

机构：

[1] UNIV TSUKUBA,INST CLIN MED,DEPT OBSTET & GYNECOL,TSUKUBA,IBARAKI 305,JAPAN

来源：

LIFE SCIENCES | 1996年 / 60卷 / 03期

关键词：

glucose; aldose reductase inhibitor (ONO-2235); nitric oxide; endothelial cell;

D O I：

10.1016/S0024-3205(96)00622-4

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

The effects of elevated glucose and aldose reductase inhibitor (ARI:ONO-2235) on nitric oxide (NO) production in cultured human umbilical endothelial cells (HUVEC) were evaluated. Aldose reductase and nitric oxide synthase(NOS) share NADPH as an obligate cofactor, therefore it is suggested that the enhanced of glucose flux (27.5 mM) by aldose reductase inhibited NO production by blunting NOS activity. However, the addition of ONO-2235 (100 mu M) prevented the inhibition of [NO2-] production. Since ARI decreases glucose-mediated inhibition of NO production in HUVEC, this agent might ameliorate endothelial function associated with diabetes.

引用

页码：PL53 / PL56

页数：4

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