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醛糖还原酶抑制剂(ARIs)的活性增加可以使细胞膜转运能力下降,渗透压改变,内环境紊乱,能量缺乏,氧化能力减弱,蛋白激酶C活化,终末糖基化产物集聚及血管内皮生长因子增加等,最终导致糖尿病并发症的发生。许多糖尿病动物模型和用半乳糖喂养的动物模型的研究结果表明,这些代谢紊乱是醛糖还原酶活性增加的结果,使用ARIs治疗,糖尿病并发症的发生可以被延缓或阻止。在过去的5年里,许多试验来
Increased activity of aldose reductase inhibitors (ARIs) may result in decreased cell membrane transport capacity, altered osmotic pressure, disturbed internal environment, lack of energy, reduced oxidative capacity, activation of protein kinase C, aggregation of terminal glycosylation products, and vascular endothelial growth Factors such as increased, eventually leading to the occurrence of diabetic complications. The findings of many animal models of diabetes and galactose-fed animal models suggest that these metabolic disorders are a result of increased aldose reductase activity and that the use of ARIs to treat diabetes complications can be delayed or prevented. In the past five years, many experiments have come