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目的 探讨氨基胍对大鼠脑缺血组织的保护作用及其作用机制。方法 采用线栓法复制大鼠中脑动脉梗死模型,缺血后给予氨基胍治疗。相应时间断头取脑,然后测定脑梗死体积、脑组织中氨基酸的含量。结果 脑梗死体积氨基胍组较缺血组明显缩小;缺血组比假手术组纹状体、海马、皮质中天门冬氨酸、谷氨酸、甘氨酸、GABA含量显著增加,给予氨基胍治疗后,天门冬氨酸、谷氨酸的含量明显降低,甘氨酸、GABA含量明显升高。结论 氨基胍降低脑组织中兴奋性氨基酸的含量,升高抑制性氨基酸的含量可能是保护脑缺血的重要机制
Objective To investigate the protective effect of aminoguanidine on cerebral ischemia in rats and its mechanism. Methods The model of middle cerebral artery occlusion was reproduced by thread occlusion, and aminoguanidine was given after ischemia. The corresponding time decapitated brain, and then determine the volume of cerebral infarction, brain tissue amino acid content. Results Compared with ischemic group, the volume of aminoguanidine group in cerebral infarction was significantly reduced. The contents of aspartate, glutamate, glycine and GABA in striatum, hippocampus and cortex in ischemic group were significantly increased compared with those in sham operated group. After treatment with aminoguanidine , Aspartic acid, glutamic acid content was significantly reduced, glycine, GABA content was significantly increased. Conclusion Aminoguanidine can reduce the content of excitatory amino acids and increase the content of inhibitory amino acids in brain tissue, which may be an important mechanism of protecting cerebral ischemia