Effects of triptolide on learning and memory abilities and NF-κB expression of hippocampus in model rats with AD
Hu Xiao
Abstract
Hu Xiao
Abstract
Objective To explore the effect of triptolide (TP) on learning and memory abilities and nuclear factor-κB (NF-κB) expression of hippocampus in model rats with Alzheimer's disease (AD). Methods 15 male SD rats were equally divided into control,AD model and TP treated groups. The AD model rats were made with bilateral microinjection of aggregated beta-amyloid protein (Aβ)1-40 into hippocampus in rats and the control rats were injected with normal saline. The TP treated group rats were administered TP intraperitoneally after microinjection of aggregated Aβ1-40 into hippocampus. Morris water maze test was used for behavioral study. The change of NF-κB expression was observed with immunohistochemical staining. Results In place navigation test,the mean escape latencies of the AD model group was obviously increased than that of control group,the mean escape latencies of the TP treated group was obviously decreased compared with the AD model group. In spatial probe test,the frequencies of passing through the platform in AD model group were obviously decreased compared with the control group,the frequencies of passing through the platform of the TP treated group were obviously increased as compared with AD model group. The cell number of the nucleus NF-κB positive staining in AD model group was higher than that of control group,the cell number of the nucleus NF-κB positive staining in TP treated group was lower than that of AD model group. Conclusions TP can inhibit the activation of hippocampal NF-κB in AD model rats,by which TP can improve the learning and memory abilities of AD model rats.
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Objective To explore the effect of triptolide (TP) on learning and memory abilities and nuclear factor-κB (NF-κB) expression of hippocampus in model rats with Alzheimer's disease (AD). Methods 15 male SD rats were equally divided into control,AD model and TP treated groups. The AD model rats were made with bilateral microinjection of aggregated beta-amyloid protein (Aβ)1-40 into hippocampus in rats and the control rats were injected with normal saline. The TP treated group rats were administered TP intraperitoneally after microinjection of aggregated Aβ1-40 into hippocampus. Morris water maze test was used for behavioral study. The change of NF-κB expression was observed with immunohistochemical staining. Results In place navigation test,the mean escape latencies of the AD model group was obviously increased than that of control group,the mean escape latencies of the TP treated group was obviously decreased compared with the AD model group. In spatial probe test,the frequencies of passing through the platform in AD model group were obviously decreased compared with the control group,the frequencies of passing through the platform of the TP treated group were obviously increased as compared with AD model group. The cell number of the nucleus NF-κB positive staining in AD model group was higher than that of control group,the cell number of the nucleus NF-κB positive staining in TP treated group was lower than that of AD model group. Conclusions TP can inhibit the activation of hippocampal NF-κB in AD model rats,by which TP can improve the learning and memory abilities of AD model rats.
Key concepts: Microinjection, Morris water navigation task, Hippocampus, Hippocampal formation, Triptolide, Saline, NF-κB, Immunohistochemistry