Abstract：Objective To study the insulin resistance rat cognitive behavior and hippocampal Alzheimer disease (AD) - like pathological change, to study the intervention effect of rosiglitazone (RSG) on the cognitive and AD- like lesions and its possible mechanism. Methods The rat models of insulin resistance were established and 20 successful models were randomly divided into the insulin resistance(IR)group(n=10) and rosiglitazone (RSG) group, each group of 10,the normal rats as control (CTL)group(n=10).The rats in RSG group were given high-protein diet with high fat and sugar +RSG 3 mg/kg/d by gavage for 4 weeks. IR group were given high-protein diet with high fat and sugar + equivalent saline by gavage for 4 weeks.CTL group were given general diet + equivalent saline by gavage for 4 weeks. The observation indexes included the blood glucose,plasma insulin levels(FINS),insulin resistance index(IRI),Morris water maze test,insulin degrading enzyme (IDE),response to insulin sialing pathway of pAKT,and Aβ protein expression in hippocampus. Results The IRI in IR group and RSG group(8.56±0.43 and 3.82±0.38)is low than that in CTL group(2.27±0.25),but in RSG group was lower than in IR group. The 4 day escape latency of rats in IR and RSG groups[(63.21±5.67)s and(37.48±5.41)s] was significantly longer than in CTL group [(24.14±5.49)s].The through the platform quadrant percentage of total time in IR and RSG groups [(21.88±3.85)% and (33.43±2.98)%] was smaller than in CTL group [(39.57±4.31)%],but RSG group is superior to IR group. The Aβ protein expressions in IR group and RSG groups (0.27±0.023 and 0.56±0.011)was stronger than that in CTL group(0.13±0.021), but RSG group is weaker than IR group. These differences were statistically significant (P<0.01 or P<0.05). Conclusions Insulin resistance rats can develop cognitive behavior decrease and aβ deposition AD like pathological changes.RSG can improve the cognitive behavior, reduce the aβ in the hippocampus of deposition, its mechanism may be through the insulin pathway mediated by IDE PI3K/AKT,to enhance IDE of aβ, thereby reducing degradation deposition.
尹黎英，刘志贤，宁青梅，陈 莉. 罗格列酮干预胰岛素抵抗大鼠认知行为及AD样病变的作用机制[J]. 武警医学, 2016, 27(5): 465-468.
YIN Liying,LIU Zhixian, NING Qingmei, and CHEN li. Mechanisms of rosiglitazone intervening in insulin resistance in cognitive-behavioral and AD-like lesion in rats. Med. J. Chin. Peop. Armed Poli. Forc., 2016, 27(5): 465-468.
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2016, Vol. 27 
