目的本研究通过高脂乳对大鼠造模观察神经炎症的激活状况,并对其形成炎症的机制进行初步研究。方法①选用SD大鼠分为空白组和模型组,模型组给予高脂乳灌胃2个月造成高脂模型。②采用ELISA方法检测脑海马、皮层、纹状体匀浆液中各组炎症因子TNF-α、IL-1β的含量。③采用Western blot方法检测了海马、皮层、纹状体各组COX2、GFAP、OX42的含量及MAPK通路中p38、ERK、JNK的活性变化。④采用免疫组化法观察GFAP标记的海马、皮层中星形胶质细胞的激活。结果实验表明在大鼠脑海马、皮层、纹状体中TNF-α、IL-1β的含量及COX2的表达水平增加,小胶质细胞和星形胶质细胞被激活,p38、ERK、JNK的活性增强。结论高脂饮食可能通过激活MAPK途径从而引起脑内炎症。
Aim To study high-fat dairy induced neuroinflammation and its mechanism.Methods ① SD rats were divided into control group and high-fat dairy group.High-fat group was administered with high-fat dairy for two months.② Effects of high-fat diet on the content of TNF-α and IL-1β in hippocampus,cortex and striatum of rats were detected by ELISA kits.③ Effects of high-fat diet on the expression of GFAP,OX42,COX2,ERK,JNK and p38 MAPK and the phosphorylation of MAPK in hippocampus,cortex and striatum of rats were determined by western blot.④ Immunohistochemictry was used to analyse of GFAP expression in hippocampus and cortex of rats.Results Levels of TNF-α,IL-1β and COX2 were increased,microglial and astrocyte were activated and the phosphorylation of MAPK was increased.Conclusion High-fat dairy may induce neuroinflammation by increasing the phosphorylation of MAPK.