论文部分内容阅读
研究脑缺血／再灌流损伤中IL－1、TNF的来源、变化规律和作用。方法用免疫组化方法检测了局部脑缺血／再灌流大鼠模型中IL－1β、TNF－α的表达。结果缺血组（I）3hlL－1β表达增多并持续至120h，缺血再灌流组（IR）0．5hIL－1β即明显增高，高峰在24h，120h已降至对照组（C）水平，阳性细胞主要为纹状体区及顶叶皮层的神经元、胶质细胞和血管内皮细胞；I组和IR组0．5hTNF－α表达增多，12h达高峰，持续至120h，阳性细胞为纹状体和缺血皮层的神经元和胶质细胞。结论IL－1β、TNF－α参与缺血／再灌流脑损伤，其来源于损伤局部的神经元、胶质细胞及血管内皮细胞，并对其作用进行了探讨。
To investigate the origin, changes and roles of IL-1 and TNF in cerebral ischemia / reperfusion injury. Methods Immunohistochemistry was used to detect the expression of IL-1β and TNF-α in rat models of focal cerebral ischemia / reperfusion. Results The expression of 3hlL-1β in ischemic group increased and continued to 120h. The level of IL-1β in ischemic reperfusion group increased significantly at 0.5h. The peak decreased to the level of control group (C) at 24h and 120h, The neurons, glial cells and vascular endothelial cells in the striatum and the parietal cortex were the main cells. The expression of TNF-α increased in 0.5h and increased to the peak at 12h in Group I and IR, and the positive cells were striatum And ischemic cortex neurons and glial cells. Conclusion IL-1β and TNF-α are involved in the ischemic / reperfusion brain injury. They are originated from the neurons, glial cells and vascular endothelial cells in local injury, and their effects are discussed.