Ischemia - reperfusion brain injury and protein synthesis inhibition.docVIP

Ischemia - reperfusion brain injury and protein synthesis inhibition.doc

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Ischemia - reperfusion brain injury and protein synthesis inhibition

 PAGE \* MERGEFORMAT 11 Ischemia / reperfusion brain injury and protein synthesis inhibition Keywords:: cerebral ischemia / reperfusion of protein synthesis inhibition Complete or incomplete cerebral ischemia / reperfusion cause permanent brain damage, although its incidence continues to in-depth understanding of the mechanism, such as the excitatory neurotransmitter theory, the mechanism of oxygen free radical damage and brain circulatory failure, etc. [1], but the therapeutic effect of these changes for the worse, and further in-depth study of cerebral ischemia / reperfusion injury mechanism is very important. In recent years, cerebral ischemia / reperfusion that occurs when the protein synthesis inhibition and its related selective vulnerability of the brain characterized by more and more attention in light of this mechanism for the treatment of cerebral resuscitation has opened up new avenues. A protein synthesis inhibition and selective vulnerability 1971, Kleihues et al [2] first reported after cerebral ischemia in brain protein synthesis inhibition and found that cat cerebral ischemia and 30 min reperfusion 4 hours brain 14C labeled amino acids in the protein the ability to reduce by 30%. Further studies have shown that the normal period of ischemia and protein synthesis, while the reperfusion period was significantly affected by inhibition of protein synthesis and found that 5 minutes of cerebral ischemia and reperfusion can result in barriers to protein synthesis [13]. Araki and other 14C clamp gerbil bilateral carotid artery experiments show that all parts of the brain in ischemia / reperfusion of protein synthesis inhibition and recovery in varying degrees, 3 minutes after ischemia in the new cortex, striatum, hippocampus and thalamus parts of the protein synthesis serious obstacles, and in the subsequent 5 to 24 hours, slow recovery, hippocampal CA1 area of the injury or even can not be restored. Morphological studies have shown that cerebral re

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