| ObjectiveIn this study, through the establishment of impaired glucose tolerance rat’s model, detect the cognitive function in rats at different time points, and the expression of key factors in different time points in rat brain tissue inflammatory pathway in rats. We analyzed the relationship between the cognition of rats and the expression of inflammatory factor function. In order to further explore the impaired glucose tolerance effects on cognitive function in rats, and its mechanism. Provide a theoretical basis for our clinical work.MethodWe selected80neonate Wistar rats (body weight180～220g). It will be randomly divided into experimental group and control group, each group40rats. The experimental group was impaired glucose tolerance group. We used high fat diet (add sugar, lard and egg yolk, based on standard full price mixed feed on heat content21.6KJ/kg) feeding the experimental group. We measured blood glucose in rats after5weeks. At5W,10W,15W,20W, water maze was used for assessment of cognition in rats. And we will use to measure nuclear transcription factor in brain tissue of rats with immunohistochemistry and in situ hybridization (factor-kappa B, NF-κB), interleukin-1β(interleukin-1, IL-1β) level. The control group, fed with normal diet, at5W,10W,15W,20W to assess cognitive function and determination of expression of inflammatory factors.ResultsWater maze test: Rats of experimental group at the beginning of the study, there was no significant difference between control group and the ability of learning and memory. With the extension of the feeding time, the rats of the experimental group gradually formed the model, all formed in fifteen weeks of feeding. After repeated monitoring of cognitive function in rats, draw the conclusion: the rats in experimental groups compared with the control group, impaired learning and memory ability, and there are significant differences in fifteenth weeks (P<0.05).HE staining: Under the light microscope, we can occasionally see apoptotic cells were round, red staining cytoplasm, nuclear chromatin aggregation of lumpy. The apoptotic cells are rapidly phagocytosed, and no inflammatory reaction, therefore in routine biopsy is not easy to be found.Determination of immunohistochemistry and in situ hybridization NF-κB: Compared with the control group, we found that the impaired glucose tolerance rats after modeling successfully the positive expression of NF-κB number. After15weeks, the difference was statistically (P<0.05), and in the20weeks was a significant difference (P＜0.01).IL-1βimmunohistochemical assay: Compared with the control group, we found that the tolerance damage in rats after modeling, the positive expression of IL-1βgradually increased.After15weeks, the difference was statistically (P<0.05), and in the20weeks was a significant difference (P<0.01).Correlation analysis:Through Pearson linear correlation and regression analysis we found, the grade of learning and memory was negatively correlated with NF-κB, IL-1βBpositive expression of rats in the experimental group, the results were statistically significant (P<0.05). We found a correlation between expression of NF-κB, IL-1βlevels and cognitive impairment.ConclusionThrough the research on the water maze test, immunohistochemistry, in situ hybridization experiments, the conclusion is glucose tolerance had significant effect on cognitive impairment in rats damaged occurrence. The mechanism may be associated with enhanced expression in rat brain nerve cells, inflammatory factor NF-κB, IL-1β. |
PDF Full Text Request