糖尿病酮症酸中毒患者脑水肿引起氧化应激损伤的研究

Role of oxidative damage in fatal brain edema in diabetic ketoacidosis patients

目的 观察氧化应激反应在急性糖尿病酮症酸中毒（DKA）致命性脑水肿（BE）中的作用.方法 研究对象为6例由我院急诊科入院治疗的1型糖尿病（T1DM）患者,对照组为6例非糖尿病死亡患者脑组织.通过检测3个不同视野的海马体或大脑普尔基涅（Purkinje）和分子层细胞CA1/CA2区,并对视野中所有神经元细胞和Purkinje细胞免疫组化染色,从而对细胞中氧化损伤标志物的集聚情况进行定量分析.结果 DKA致命性脑水肿患者大脑海马体锥体神经元细胞中8-羟基鸟嘌呤（8OHG）、4-羟基壬烯醛（HNE）、血红素加氧酶（HO-1）的含量显著高于对照组.而小脑中,只有8OHG在Purkinje细胞和小脑分子层其他细胞中含量升高.结论 氧化应激反应是导致T1 DM脑病的重要病因之一.

Objective To observe the role of oxidative stress in an acute setting,specifically in fatal brain edema （BE） associated with diabetic ketoacidosis （DKA）.Methods The present study included 6 patients with type 1 diabetes mellitus （T1DM） in emergency department of our hospital,6control cases of non diabetes death of brain tissue of patients.Three fields of the CA1/CA2 region of the hippocampus or of the cerebellum inclusive of the Purkinje and molecular layers as well as all neurons or Purkinje cells in the fields were observed and measured.The cellular accumulation of the related oxidative damage markers was quantified.Results We found that increased levels of 8-hydroxyguanosine（8OHG）,4-hydroxynonenal （HNE）,and heme oxygenase-1 （HO-1） in the pyramidal neurons of the hippocampus of DKA BE in comparison to controls.However,in the cerebellum,only 8OHG was increased in the Purkinje cells and other cells of the molecular layer.Conclusion These results display a role for oxidative stress in the pathogenesis of T1DM encephalopathy.