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代谢综合征大鼠脑神经元和微血管损伤炎性反应机制的研究 被引量:5

Inflammatory Mechanism of Brain Neuron and Microvascular Injury of Rats with Metabolic Syndrome
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摘要 目的:通过对老龄代谢综合征大鼠对相关炎性因子表达的研究,探讨老年代谢综合征神经元和微血管损伤的病理生理特点。方法:用喂养法建立代谢综合征大鼠动物模型,分为青年正常组、青年模型组、老龄正常组、老龄模型组,观察各组大鼠血清、组织中TNF-α、IL-6表达的变化。结果:青年模型组、老龄模型组大鼠血清炎性因子TNF-α、IL-6水平均分别较青年正常组和老龄正常组显著上升(P<0.01),青年模型组较老龄模型组上升更明显(P<0.01);青年模型组、老龄模型组大鼠脑组织炎性因子TNF-α、IL-6的表达,均分别较青年正常组和老龄正常组明显升高(P<0.01),老龄模型组较青年模型组增高更明显(P<0.01)。结论:采用高脂、高糖、高盐复合饲料喂养方法可以复制代谢综合征大鼠模型,该模型炎性因子TNF-α、IL-6水平明显增加,提示TNF-α、IL-6参与了MS及其靶器官损伤的炎性反应。 Objective:To discuss the physiological and pathological characters of brain neuron and microvascular injury of gerontic metabolic syndrome by studying the expression of inflammatory factors of gerontic rats with metabolic syndrome.Methods:metabolic syndrome model rats were divided into the young normal group,young model group,gerontic normal group and the gerontic model group.Observed the expreeion change of blood serum,TNF-α and IL-6 in the tissues of each group.Results:The serum inflammatory factors TNF-α and IL-6 of the young model group and the gerontic model group increased significantly in comparison with those of the young normal group and gerontic normal group (P〈0.01),the young model group bad the more obvious increase than the gerontic model group (P〈0.01).The inflammatory factors TNF-α and IL-6 in the cerebral tissues of the young model group and the gerontic model group increased significantly in comparison with those of the young normal group and gerontic normal group (P〈0.01),the gerontic model group had the more obvious increase than the young model group (P〈0.01).Conclusion:The feeding method with high-fat,high-sugar and high-salt feed can duplicate metabolic syndrome model rats,and the level of its inflammatory factors TNF-α and IL-6 may increase obviously,which suggests that TNF-α and IL-6 have been involved in the inflammatory raction of MS and its target-organ damage.
出处 《河南中医》 2008年第9期38-40,共3页 Henan Traditional Chinese Medicine
关键词 代谢综合征 神经元 炎性因子 大鼠 metabolic syndrome neuron inflammatory factors rats
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