The Effect Of Insulin On AGEs、InsR Expression In Rats With Diabetic Encephalopathy

Objective: To observe the cognitive function of diabetic rats in1month and3months, and the changes of advanced glycation end product（sAGEs）、insulin receptors（InsR） expression in brain, explore the effect of AGEs、InsR in diabetic rats andwhether insulin can be applied to prevent diabetic cognitive impairment.Methods:36healthy adult male SD （Sprague-Dawley） rats, weight180-240g,were divided into3groups randomly: diabetic group （n=12）, insulin treatment group（n=12）and control group（n=12）, and then each group was divided into2groupsrandomly:1month group and3months group. Diabetic group and insulin treatmentgroup rats were induced by streptozotocin injection. Fixed time to measure bloodglucose of all rats two times a week. Insulin treatment group rats were injected insulindaily, and we adjusted insulin dosage according to the blood glucose level to ensureblood glucose in normal range. All the rats underwent the test of Morris water maze in1month and3months. To evaluate the cognitive function, after which the expression ofAGEs and InsR in brain were observed.Results:1.1month group of diabetic rats appeared cognitive impairment, the expressionof AGEs increased and InsR reduced, compared with the control group, hasstatistical difference(P <0.05).2.3months group of diabetic rats, the cognitive impairment was obviouslyaggravated, the expression of AGEs increased and InsR reduced moresignificantly, compared with1month diabetic group, has statisticaldifference(P <0.05).3.1month group of insulin treatment rats with no significant cognitiveimpairment, brain tissue with a little expression of AGEs, compared with control group and1month diabetic group, has statistical difference(P <0.05);the expression of InsR were reduced slightly, compared with the control group,with no difference(P>0.05), compared with the1month diabetic group, hasstatistical difference(P <0.05).4.3months group of insulin treatment rats appeared cognitive impairment, theexpression of AGEs increased and InsR reduced obviously, compared withcontrol group, has statistical difference(P <0.05), compared with1monthgroup of insulin treatment rats, has statistical difference(P <0.05), comparedwith3months group of diabetic rats, with no statistical difference(P>0.05).Conclusion:1．Diabetic cognitive impairment is closely related to AGEs and InsR, theincreased AGEs expression and reduced InsR expression may contribute todiabetic cognitive impairment.2．Early intervention of insulin, has protective effect on the brain, can reduce thedestruction of the InsR and reduce the AGEs expression, then delay cognitiveimpairment.3．As the extension of the duration, the insulin treatment group rats still showedcognitive impairment, which suggests that long-term application of insulin cannot prevent the occurrence of cognitive impairment, and that it may beassociated with the excessive deposition of AGEs and progressive reduction ofInsR. Mechanisms need to be further explored.