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Influence of diabetes mellitus on cerebral ischemia and reperfusion injury.

机译：糖尿病对脑缺血和再灌注损伤的影响。

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摘要

Diabetes mellitus aggrevates and worsens the brain damage caused by global or focal cerebral ischemia. The purpose of our study was to explore what is the underlying mechanism of the exaggerated brain damage caused by diabetic ischemia. In our experiments we investigated whether there is a difference in the activation of the mitochondria-dependent apoptotic pathway after ischemic injury in diabetic rats compared to non-diabetic animals. In further experiments we examined whether increased free radical production and activation of astrocytes contribute to the exaggerated brain damage after diabetic ischemia compared to non-diabetic ischemia. Finally, we investigated the heat shock protein expression and synthesis in hyperglycemic ischemia. Early activation of apoptotic cell death pathway in diabetic animals was observed. The results show that the production of free radicals such as superoxide anion, nitric oxide and peroxynitrite are stimulated in neurons after diabetic ischemic injury. In astrocytes only nitric oxide production was enhanced. These data suggest that diabetic ischemia increases peroxynitrite production in neurons by enhancing the formation of superoxide since peroxynitrite is derived from the reaction of NO and superoxide. As a reaction to the increased stress caused by hyperglycemia enhanced the heat shock protein expression and synthesis in neuronal cells. Finally, we detected reactive astrogliosis in both ischemic groups, although in the diabetic animals damage of astrocytes was observed early after the ischemic injury. These results draw attention to the enhanced intracellular events leading to cell damage may further limit the time-window of the effective therapy, if the patient suffer from diabetes mellitus.
机译：糖尿病会加剧并加剧由整体或局灶性脑缺血引起的脑损伤。我们研究的目的是探讨糖尿病性缺血引起的夸大性脑损伤的潜在机制是什么。在我们的实验中，我们调查了糖尿病大鼠与非糖尿病动物相比，缺血性损伤后线粒体依赖性凋亡途径的激活是否存在差异。在进一步的实验中，我们检查了与非糖尿病性缺血相比，糖尿病性缺血后星形胶质细胞自由基产生和活化的增加是否导致了过度的脑损伤。最后，我们研究了高血糖缺血中热休克蛋白的表达和合成。观察到糖尿病动物中凋亡细胞死亡途径的早期激活。结果表明，糖尿病缺血性损伤后神经元中自由基的产生受到刺激，如超氧阴离子，一氧化氮和过氧亚硝酸盐。在星形胶质细胞中，仅一氧化氮产生增加。这些数据表明，糖尿病性缺血通过增强超氧化物的形成来增加神经元中过氧亚硝酸盐的产生，因为过氧亚硝酸盐源自NO和超氧化物的反应。作为对由高血糖引起的压力增加的反应，增强了神经细胞中热休克蛋白的表达和合成。最后，尽管在糖尿病动物中，在缺血性损伤的早期观察到星形胶质细胞的损伤，但我们在两个缺血性组中均检测到了反应性星形胶质增生。这些结果引起人们对引起细胞损伤的细胞内事件增强的关注，如果患者患有糖尿病，则可能进一步限制有效治疗的时间范围。

著录项

  • 作者

    Muranyi, Marianna.;

  • 作者单位

    Semmelweis Egyetem (Hungary).;

  • 授予单位 Semmelweis Egyetem (Hungary).;
  • 学科 Health Sciences Medicine and Surgery.
  • 学位 Ph.D.
  • 年度 2006
  • 页码 91 p.
  • 总页数 91
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 R501;R601;
  • 关键词

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