以Fat-1转基因小鼠和野生型C57BL/6小鼠为研究对象,经侧脑室注射脂多糖(lipopolysaccharide,LPS)诱导中枢炎症模型,测定抑郁样行为糖水偏好度和悬尾实验、腹腔巨噬细胞活性及其吞噬能力、脑炎症小胶质细胞的标记物CD11b基因与蛋白的表达水平,用以研究Fat-1对LPS诱发的炎症和抑郁样行为的作用.结果表明:在野生型小鼠中,LPS降低小鼠糖水偏好度,延长悬尾静止不动时间,增加腹腔巨噬细胞的活性和吞噬能力,上调CD11b基因和蛋白表达水平;而LPS不能引起Fat-1转基因小鼠出现上述类似变化.侧脑室注射LPS可引起野生型小鼠炎症反应和抑郁样行为,而Fat-1转基因小鼠可通过脑内和体内合成n-3 PUFAs抵抗LPS诱发的上述抑郁样变化.%The wild type C57BL/6 mice and transgenic mice Fat-1 are used as the research objects. After 24 h central administration of lipopolysaccharide (LPS) and saline, sucrose preference, immobility times of tail suspension test, activity and phagocytosis of macrophages, CD11b gene and protein expression level were measured to study the potential anti-inflammatory effect of n-3 polyunsaturated fatty acids produced in the brain. The results showed that after LPS was injected to the C57BL/6 mice, the sucrose preference was significantly decreased (P < 0.05), the tail suspension immobility time was significantly increased (P < 0.01), the activity of peritoneal macrophages (P < 0.01) and phagocytosis (P< 0.05) significantly increased, CD11b gene (P < 0.01) and protein expression level (P < 0.05) increased significantly, while LPS-induced change was reversed in Fat-1 mice. It can be seen that the injection of LPS to lateral ventricle can cause depression like symptoms in mice, while Fat-1 mice can improve the depression like symptoms induced by LPS producing n-3 PUFAs in the brain and the body.
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