Department of Anatomy and Cell Biology, College of Veterinary Medicine and Research Institute for Veterinary Science, Seoul National University, Seoul 151-742, South Korea.
Neurochem Res. 2011 Jan;36(1):117-28. doi: 10.1007/s11064-010-0280-6. Epub 2010 Oct 6.
Because it appears that oxidative stress and inflammation are implicated with disease pathogenesis in the diabetic brain, many researchers have used streptozotocin (STZ)-induced diabetic animals to study superoxide production and the effects of superoxide scavengers like Cu,Zn-superoxide dismutase (SOD1). However, many studies have been conducted without considering temporal changes after STZ injection. Interestingly, though SOD activities were not significantly different among the groups, SOD1 and 4-hydroxy-2-nonenal (4-HNE) immunoreactivities were significantly enhanced at 3 weeks after an STZ injection (STZ3w) versus only marginal levels in sham controls, whereas microglial activity was remarkably reduced in injected rats at this time. However, SOD1 immunoreactivity and microglial activities were only at the sham level at STZ4w. The present study provides important information concerning cell damage by ROS generated by STZ. Microglial response was found to be inactivated at STZ3w and neuronal cells (NeuN) showed a non-significant tendency to be reduced in number at STZ4w except in the dentate gyrus. We speculated that the above oxidative stress-related events should be accomplished at STZ3w in the brains of STZ-induced diabetes animal models. Therefore, the aim of the present study was to investigate chronological changes in SOD1 immunoreactivity associated with lipid peroxidation and inflammatory responses in the hippocampi of STZ-induced type I diabetic rats.
由于氧化应激和炎症与糖尿病大脑的发病机制有关，许多研究人员使用链脲佐菌素（STZ）诱导的糖尿病动物来研究超氧化物的产生以及超氧化物清除剂（如 Cu，Zn-超氧化物歧化酶[SOD1]）的作用。但是，许多研究都没有考虑到 STZ 注射后的时间变化。有趣的是，尽管 SOD 活性在各组之间没有明显差异，但 SOD1 和 4-羟基-2-壬烯醛（4-HNE）免疫反应性在 STZ 注射后 3 周（STZ3w）时明显增强，而假对照中仅略有水平，而此时注射大鼠中的小胶质细胞活性明显降低。但是，在 STZ4w 时，SOD1 免疫反应性和小胶质细胞活性仅处于假对照水平。本研究提供了有关 STZ 产生的 ROS 引起的细胞损伤的重要信息。发现小胶质细胞反应在 STZ3w 时失活，并且神经元细胞（NeuN）在 STZ4w 时数量减少，但无统计学意义，除了在齿状回。我们推测，上述与氧化应激相关的事件应在 STZ 诱导的糖尿病动物模型的大脑中在 STZ3w 时完成。因此，本研究的目的是研究 SOD1 免疫反应性与 STZ 诱导的 1 型糖尿病大鼠海马中脂质过氧化和炎症反应的时间变化的关系。
