Effect of Helicid on cognitive function in Aβ1-42 induced Alzheimer's disease model rats
Objective:To investigate the effects of helicid(HEL)on cognitive function of Aβ1-42 induced Alzhei-mer's disease(AD)rats.Methods:Twenty-four healthy male SD rats were randomly divided into Normal saline(NS)group,Aβ1-42+NS group,Aβ1-42+HEL group and HEL group,with 6 rats in each group.The AD model was estab-lished by injecting Aβ1-42(5 μg/μL)into the hippocampus of brain stereotaxic injection.After 3 days of injection,Aβ1-42+NS group and Aβ1-42+HEL group were given normal saline and Helicid(50 mg/kg)for 4 weeks.NS group and HEL group were given normal saline and Helicid(50 mg/kg)for4 weeks,respectively.After treatment,the behav-ior and cognitive ability of rats in each group were evaluated by Morris water maze test.HE staining was used to detect the morphological changes of Hippocampal CA1 cells in each group.The expression of nuclear factor-κB(NF-κB)in hippocampal CA1 region was detected by Immunohistochemistry.Western blot was used to detect the protein expressions of(amyloiol protein precursor,APP),NF-κB and TNF-α in Hippocampal CA1.Results:Aβ1-42+NS group's es-cape latency was increased significantly more than the NS group,through the original times and stay in the original plat-form quadrant were significantly decreased.Hippocampal CA1 cell morphology showed obvious pyknosis;The expres-sions of APP,NF-κB and TNF-α were obviously increased(P＜0.05).Compared with the Aβ1-42+NS group,the escape latency of rats in the Aβ1-42+HEL group was obviously decreased,the number of crossing the platform and the residence time in the target quadrant were significantly increased.Pyknosis of nucleus in Hippocampal CA1 was im-proved.The expressions of APP,NF-κB and TNF-α were obviously decreased(P＜0.05).There was no significant difference in Morris water maze results between NS group and HEL group.APP,NF-κB and TNF-α proteins had no distinct changes in Hippocampal CA1.Conclusions:Helicid can improve the cognitive function of AD rats induced by Aβ1-42,which may be related to the inhibiting the expression of APP,NF-κB and TNF-α proteins.
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