ObjectiveTo observe the effect of rosiglitazone on cognitive function, serum high sensitive C reactive protein (hs-CRP) and expression of nuclear factor-κB (NF-κB), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) in hippocampal tissues of senile diabetic rats. MethodsThirty aged Wistar rats (20-22 months) were randomly divided into normal control group (n=6), diabetic model group (n=12), and rosiglitazone treatment group (n=12). Streptozotocin-induced diabetic rat model was established. In the rosiglitazone treatment group, the rats were treated with rosiglitazone 4mg/kg/d for 8 weeks. The cognitive function of rats was evaluated with the Morris water maze test. Serum hs-CRP was detected by ELISA. The expression of NF-κB in hippocampal tissues was detected by western blot and IL-6 and TNF-α by Real-time PCR. ResultsThe Morris water maze test showed that escape latency was longer in the rosiglitazone treatment group and the diabetic model group than that in the control group (P<0. 05). Compared with the diabetic model group, the rosiglitazone treatment group showed a significant decrease in the average time of escape latencies (P<0.05), and an increased percentage of time spent in the central area and the more times navigating the original platform position (P<0.05). Serum hs-CRP and the expression of NF-κB, IL-6 and TNF-α in the rosiglitazone treatment group and the diabetic model group was significantly higher than those in the control group (P<0.01). Compared with the diabetic model group, serum hs-CRP and the expression of NF-κB, IL-6 and TNF-α in the rosiglitazone treatment group was decreased (P<0.05). ConclusionCognitive impairment in senile diabetic rats is associated with serum hs-CRP. The cognitive function can be improved with rosiglitazone treatment. The protective mechanisms may be related to the decrease of serum hs-CRP, inhibition of NF-κB signal and down-regulation of the expression of IL-6 and TNF-α in hippocampal tissues.