Okuda Y, Kawashima K, Suzuki S, Asakura Y, Asano M, Tsurumaru K, Dai H, Tachi Y, Bannai C, Saitoh M, Yamashita K
Department of Internal Medicine, Institute of Clinical Medicine, University of Tsukuba, Japan.
Life Sci. 1997;60(3):PL53-6. doi: 10.1016/s0024-3205(96)00622-4.
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 microM) 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.
评估了高糖和醛糖还原酶抑制剂（ARI：ONO-2235）对培养的人脐静脉内皮细胞（HUVEC）中一氧化氮（NO）生成的影响。醛糖还原酶和一氧化氮合酶（NOS）共用NADPH作为必需的辅因子，因此有人提出，醛糖还原酶增强的葡萄糖通量（27.5 mM）通过削弱NOS活性来抑制NO生成。然而，添加ONO-2235（100 microM）可防止[NO2-]生成受到抑制。由于ARI可降低葡萄糖介导的HUVEC中NO生成的抑制作用。这种药物可能会改善与糖尿病相关的内皮功能。
