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高血糖与脑缺血后神经损伤的恶化密切相关。因高血糖而增加的氧化应激是脑损伤加重的重要因素,超氧化物、一氧化氮以及过氧化亚硝酸盐等自由基的生成起了重要的损伤作用。超氧化物可激活多元醇、晚期糖基化终产物、蛋白激酶C和己糖胺途径,促进脑损伤的发展;一氧化氮因神经保护作用的减弱和细胞毒性作用的增强而加剧脑缺血损伤。活性氧基团和活性氮基团可直接造成脂质、蛋白质和DNA的氧化损伤。本文综述了高血糖脑缺血过程中氧化应激的来源及其损伤机制,为糖尿病患者脑缺血损伤的防治提供帮助。
Hyperglycemia is closely related to the deterioration of nerve injury after cerebral ischemia. Increased oxidative stress due to hyperglycemia is an important factor in aggravating brain injury. The formation of free radicals such as superoxide, nitric oxide and peroxynitrite play an important role in injury. Superoxide activates polyols, advanced glycation end products, protein kinase C and hexosamine pathways, promoting the development of brain injury; nitric oxide exacerbates cerebral ischemic injury due to a decrease in neuroprotection and an increase in cytotoxicity . Reactive oxygen and reactive nitrogen groups can directly cause oxidative damage to lipids, proteins and DNA. This review summarizes the sources of oxidative stress and its mechanism of injury during hyperglycemic cerebral ischemia, which may be helpful in the prevention and treatment of cerebral ischemic injury in diabetic patients.