Cognition Disorders Of Impaired Glucose Regulation Rat With The Expression Of NF-κBp65and TNF-α

Objective:Impaired glucose tolerance model rats were made by high fat and sugar diet; To explore the function of NF-k B and TNF-α in the rat brain of cognition disorders, and discuss the relationship between impaired glucose tolerance and cognition disorders from the perspective of inflammatory mechanism.Methods:By random assignment,56wistar male rats in SPF level were conducted contast group and experimental group, and each group has28rats. Contast group recevied standard diet while experimental group recevied high fat diet, and raise a total of20weeks. Monitoring the change of rats’weight and adjusting control group feed intake according to experimental group’s. Glucose tolerance test was started from the8th week, and continued on a bi weekly basis. The test blood-sugar content was performed at five time points(empty stomach、0h、0.5h、1h、2h、3h),which was taken from the rat tail. Rat of fasting blood glucose (6.2-7.5mmol/1) or two hour postprandial blood glucose(7.9-10.4mmol/1) was relegated to IGR model successfully. Water maze test was taken by the control group and the experimental group in5W,10W,15W,20W respectively, including adaptive training, navigation training, spatial probe test. The water maze test data was analysed with SPSS20.0software, and comparisons between groups were tested by multiple analysis of variance for repeated measurements and q test with format of x±s, supposing P=0.05.28rats in control group(mark A) and28rats in experimental group(mark B) were decapitated at five time point(5W、10W、15W、20W),7rats were decapitated each time in both group with order marked A1, B1, A2, B2, A3, B3, A4, B4. After all rat brain tissue soaked for24h in4%PFA, they were conservated by paraffin-section method. The expression of NF-kB、TNF-α factor in rat brain were detected using immunohistochemistry and in situ hybridizational. Five different microscope view of200*without overlapping each other were choosen in each parafin section, and average optical density value were used to reflect the result. Data of water maze test and expression of NF-kB, TNF-α were analyzed with Pearson’s correlation by SPSS20.0software.Result:Rat’s weight increased with years, and compared with the age-matched control group, the experimental group’s weight increased obviously (P<0.05).Compared with the control group, the sugar in blood had no significant difference in the first12week(P>0.05),while it increased obviously in the following weeks(P<0.05). As time went on, IGR rats were increased gradually, all rats in experimental group turned into IGR rats in15weeks. Water maze test shows that compared with contrast group, the ability of learning and memory were significantly increased (P<0.05) in the fifth week, while the ability in experimental group were meaningfully decreased step by step after10th weeks,and were decreased obviously at20th week(P<0.01).Compared with contrast group, the difference at the experision of NF-k B、TNF-α was not significant at5W and10W, while it was slight at15W(P<0.05) and significant at20W (P<0.01). After10W,the expression of NF-k B、TNF-α in immunohistochemistry and in situ hybridization increased progressively, and there was a difference among experimental groups(P<0.05). The training times for rats to reach the learning standard were correlated positively with the expression of NF-kB and TNF-α in cortex of experimental group, but not in contrast group.Conclusions:High fat diet establish a stable IGR animal model, which could be applied to IGR style. As time went on, the blood sugar of high fat diet rats were increased gradually. The findings suggested that high fat diet and aging had ralative with IGR. With the successful model come up, the rats’ability of study and memory debased. The training times for rats to reach the learning standard were correlated positively with the high expression of NF-kB and TNF-a in cortex of experimental group, that was to say the high expression of NF-kB and TNF-a may be involved in cognition disorder process. The of NF-kB他TNF-α in rat brain may the main factor of IGR to cognition disorder.