In the ApoE^-/- mouse model of atherosclerosis （AS） stable plaque, the expression and location of intracellular tissue factor （TF） in the cellular components of AS stable plaque were investigated in order to explo...In the ApoE^-/- mouse model of atherosclerosis （AS） stable plaque, the expression and location of intracellular tissue factor （TF） in the cellular components of AS stable plaque were investigated in order to explore the cellular mechanism of AS thrombosis. Pathological changes of the stable plaque were observed under a microscope. The expression of TF protein was examined in aortic stable plaque of mice by using immunohistochemistry. Color image planimetric system was used to analyze the histological components of the stable plaque and the TF distribution. Under the confocal microscope, the intracellular TF location in the stable plaque of mice was observed. The results showed the cellular area was the major part of stable plaque （67.36%±6.52%, P〈0.01）. The percentage of total area occupied by cellular area was significantly larger than atheromatous gruel and acellular area （P〈0.01）. Macrophages and smooth muscle cells （SMC） were major cells in the cellular area. The percentage of total area occupied by SMC was significantly larger than by macrophages （P〈0.01）. Multiple linear regression analysis showed there was a positive correlation between TF area and SMC area （r=0.616, P=-0.008）, and no correlation was found between TF area and macrophage area （r=0.437, P=0.08）. Pictures of color image planimetric analysis of TF and SMC were merged to highlight areas with co-localization （yellow）, it was concluded that the process could be a cell-mediated TF expression in the stable plaque. SMC may be the major source of TF in AS without plaque rupture.展开更多
目的探讨高热量饮食和年龄对载脂蛋白E基因敲除(ApoE^(-/-))小鼠脑功能的影响。方法选取8月龄成年ApoE^(-/-)小鼠和18月龄老年ApoE^(-/-)小鼠共20只,随机分为正常饮食成年组、正常饮食老年组、高热量饮食成年组、高热量饮食老年组,每组...目的探讨高热量饮食和年龄对载脂蛋白E基因敲除(ApoE^(-/-))小鼠脑功能的影响。方法选取8月龄成年ApoE^(-/-)小鼠和18月龄老年ApoE^(-/-)小鼠共20只,随机分为正常饮食成年组、正常饮食老年组、高热量饮食成年组、高热量饮食老年组,每组5只。正常饮食成年组、正常饮食老年组小鼠喂食实验室标准饲料,高热量饮食成年组、高热量饮食老年组小鼠喂食高脂饲料,干预8周。用体质量监测和葡萄糖耐量实验测试小鼠体质量、血糖变化,核磁共振波谱检测海马和下丘脑N-乙酰天冬氨酸(NAA)、胆碱(Cho)含量,Y迷宫和旷场实验检测认知功能,Western blot检测脑组织突触体相关蛋白25(SNAP-25)、突触素(synaptophysin)、突触后致密蛋白95(PSD-95)、诱导型一氧化氮合酶(iNOS)、白细胞介素1β(IL-1β)表达。结果与正常饮食成年组比较,高热量饮食成年组海马NAA、下丘脑Cho和NAA、自发交替率、SNAP-25、synaptophysin、PSD-95表达降低,差异有统计学意义(P<0.05,P<0.01),iNOS、IL-1β表达升高,差异有统计学意义(P<0.01);与正常饮食成年组比较,正常饮食老年组海马NAA、下丘脑Cho、SNAP-25、synaptophysin、PSD-95表达降低(P<0.05,P<0.01),iNOS、IL-1β表达升高(P<0.01);与正常饮食老年组比较,高热量饮食老年组海马和下丘脑Cho和NAA、中心路程/总路程、SNAP-25、synaptophysin、PSD-95表达降低(P<0.05,P<0.01),iNOS、IL-1β表达升高(P<0.01);与高热量饮食成年组比较,高热量饮食老年组海马NAA、中心路程/总路程、平均速度、synaptophysin表达降低(P<0.05,P<0.01),iNOS、IL-1β表达升高(1.61±0.10 vs 1.35±0.13,2.04±0.08 vs 1.54±0.11,P<0.05,P<0.01)。结论高热量饮食导致ApoE^(-/-)小鼠代谢障碍和神经炎症,抑制突触蛋白表达引起认知功能障碍;长期高热量饮食和年龄增加促进ApoE^(-/-)小鼠脑功能衰退。展开更多
基金supported by a grant from the National Natural Sciences Foundation of China(No.30200109)
文摘In the ApoE^-/- mouse model of atherosclerosis （AS） stable plaque, the expression and location of intracellular tissue factor （TF） in the cellular components of AS stable plaque were investigated in order to explore the cellular mechanism of AS thrombosis. Pathological changes of the stable plaque were observed under a microscope. The expression of TF protein was examined in aortic stable plaque of mice by using immunohistochemistry. Color image planimetric system was used to analyze the histological components of the stable plaque and the TF distribution. Under the confocal microscope, the intracellular TF location in the stable plaque of mice was observed. The results showed the cellular area was the major part of stable plaque （67.36%±6.52%, P〈0.01）. The percentage of total area occupied by cellular area was significantly larger than atheromatous gruel and acellular area （P〈0.01）. Macrophages and smooth muscle cells （SMC） were major cells in the cellular area. The percentage of total area occupied by SMC was significantly larger than by macrophages （P〈0.01）. Multiple linear regression analysis showed there was a positive correlation between TF area and SMC area （r=0.616, P=-0.008）, and no correlation was found between TF area and macrophage area （r=0.437, P=0.08）. Pictures of color image planimetric analysis of TF and SMC were merged to highlight areas with co-localization （yellow）, it was concluded that the process could be a cell-mediated TF expression in the stable plaque. SMC may be the major source of TF in AS without plaque rupture.
文摘目的探讨高热量饮食和年龄对载脂蛋白E基因敲除(ApoE^(-/-))小鼠脑功能的影响。方法选取8月龄成年ApoE^(-/-)小鼠和18月龄老年ApoE^(-/-)小鼠共20只,随机分为正常饮食成年组、正常饮食老年组、高热量饮食成年组、高热量饮食老年组,每组5只。正常饮食成年组、正常饮食老年组小鼠喂食实验室标准饲料,高热量饮食成年组、高热量饮食老年组小鼠喂食高脂饲料,干预8周。用体质量监测和葡萄糖耐量实验测试小鼠体质量、血糖变化,核磁共振波谱检测海马和下丘脑N-乙酰天冬氨酸(NAA)、胆碱(Cho)含量,Y迷宫和旷场实验检测认知功能,Western blot检测脑组织突触体相关蛋白25(SNAP-25)、突触素(synaptophysin)、突触后致密蛋白95(PSD-95)、诱导型一氧化氮合酶(iNOS)、白细胞介素1β(IL-1β)表达。结果与正常饮食成年组比较,高热量饮食成年组海马NAA、下丘脑Cho和NAA、自发交替率、SNAP-25、synaptophysin、PSD-95表达降低,差异有统计学意义(P<0.05,P<0.01),iNOS、IL-1β表达升高,差异有统计学意义(P<0.01);与正常饮食成年组比较,正常饮食老年组海马NAA、下丘脑Cho、SNAP-25、synaptophysin、PSD-95表达降低(P<0.05,P<0.01),iNOS、IL-1β表达升高(P<0.01);与正常饮食老年组比较,高热量饮食老年组海马和下丘脑Cho和NAA、中心路程/总路程、SNAP-25、synaptophysin、PSD-95表达降低(P<0.05,P<0.01),iNOS、IL-1β表达升高(P<0.01);与高热量饮食成年组比较,高热量饮食老年组海马NAA、中心路程/总路程、平均速度、synaptophysin表达降低(P<0.05,P<0.01),iNOS、IL-1β表达升高(1.61±0.10 vs 1.35±0.13,2.04±0.08 vs 1.54±0.11,P<0.05,P<0.01)。结论高热量饮食导致ApoE^(-/-)小鼠代谢障碍和神经炎症,抑制突触蛋白表达引起认知功能障碍;长期高热量饮食和年龄增加促进ApoE^(-/-)小鼠脑功能衰退。
