大鼠慢性乙醇中毒脑组织微管相关蛋白Tau的表达与外伤性蛛网膜下腔出血致死机制的关系

Relationship between the expression of Tau protein and mechanism of traumatic subarachnoid haemorrhage in chronic alcoholic rat brain

目的：观察大鼠慢性乙醇中毒后轻微伤脑组织微管相关蛋白（Tau蛋白）的表达，探讨酗酒与外伤性蛛网膜下腔出血（TSAH）死亡机制的相关性。方法：雄性SD大鼠随机分为饮水打击组、饮酒组、饮酒打击组，饮酒组（52％v／v北京红星二锅头）连续灌胃4周，打击组予脑震荡性打击，各组大鼠脑组织行H—E染色、免疫组织化学显色，并用图像分析系统对检测结果进行分析。结果：随着饮酒时间延长，大鼠逐渐出现慢性乙醇中毒改变，TSAH发生率和死亡率增高，脑干周围多见TSAH，神经元变性、坏死，神经纤维疏松水肿，神经骨架纤维崩解；脑干、小脑、海马、额叶等部位Tau IOD值增高。结论：慢性乙醇中毒脑组织在轻微损伤的情况下可引起脑神经纤维细胞骨架的形态结构破坏，脑白质萎缩、神经突起数量减少，推测慢性乙醇中毒后轻微的外伤可能参与了TSAH病理生理过程。

Objective： To explore the correlation of chronic alcoholism and the mechanism of death associated with traumatic sub- arachnoid haernorrhage （TSAH）, and to observe the Tan protein expression in the brain after chronic alcoholism in rats~ Methods： Male SD rats were randomly divided into three groups： the chronic water group with strike, the chronic alcoholism group, and the chronic alcoholism group with strike. Four weeks later, the rats were sacrificed and sagittal sections of the brain were prepared for routine paraffin serial sections, H-E and Tau protein immunohistochemical staining. The pathological changes were analyzed by computer image analysis system. Results： With the drinking time extending, the rats showed a gradual change in chronic alcoholism. In the chronic alcoholism group with strike, the neurons and glial cells were in a high degree of hydropic degeneration; with the perivitelline space expanding, more nucleus pyknosis dissolved and disap- peared. The nerve fibers were loose and swollen, and cell gap was widened with irregular thickening, distort, break, and lo- cal swelling. In the chronic alcoholism strike group, Tau IOD sum value in the brainstem, cerebellum, hippocampus, frontal lobe and other parts were significantly higher. Conclusion： The chronic alcoholism brain tissue in slight injury could cause the damage of the cytoskeleton morphological structure of the nerve fibers in CNS, reduce the neurite number and white mat- ter atrophy. The chronic alcoholism poisoning after slight trauma may be involved in the TSAH pathophysiological process.