论文部分内容阅读
Objective: The present study was designed to investigate the neuroprotective potential of lycopene on inflammatory response and TLR4 pathway of choroid plexus in β-amyloid induced model of Alzheimers disease.Methods: 40 adult SD rats(Body weight:250±18.7g)were randomly divided into five groups(n= 8): control,AD model,AD+lycopene(ig.5mg/kg.d),AD+lycopene(ig.10mg/kg.d)and lycopene group.The rats were adapted for one week prior to the present experiment.8μg β-amyloid(Aβ1-42)was administered through intracerebroventricular(ICV)by using stereotaxic instrument in AD group and the AD+lycopene group rats bilateral hippocampus,and the control and lycopene groups with equal saline.All the rats were trained on a Morris water maze test after 2,3,4,5 weeks to identify leaming and memory ability of the rats.The rats were sacrificed and the blood were prepared for the quantification of TNF-α,IL-1β and IL-6β level by ELISA.The expression of TLR4,NF-κB p65 mRNA and protein was detected by RT-qPCR and western blot.Western blot was also used to detect the expression of PS-1 and β-APP in hippocampus.Results: Compared with the control group,the latent period of escape and activity time in AD group was significantly longer(P< 0.05).But the rats performed better in AD+lycopene groups than in AD group(P< 0.05).Compared with the control group,the level of TNF-α,IL-1β and IL-6β in AD group was significantly incresed(P< 0.05),but significantly decresed in AD+lycopene groups(P< 0.05).Compared with the control group,the expression of TLR4,NF-κB p65 mRNA and protein were also significantly incresed(P< 0.05),but significantly decresed in AD+lycopene groups(P< 0.05).Along with this,compared with the control group,the expression of PS-1 and β-APP in hippocampus were significantly incresed(P< 0.05),but were reversed on lycopene treatment(P< 0.05).Conclusion: Collectively,these observations provide an evidence for beneficial effect of lycopene supplementation in β-amyloid-induced Alzheimers disease and lycopene has anti-inflammatory effects against Aβ-triggered choroid plexus via a mechanism that involves the TLR4-mediated NF-κB p65 signaling cascade.