Effects of triptolide on the expression of inducible nitric oxide synthase and synaptic ultrastructure in hippocampus of model rats with Alzheimer's disease
Hu Xiao
Abstract
Hu Xiao
Abstract
Objective To explore the effects of triptolide on the expression of inducible nitric oxide synthase( i NOS) and synaptic ultrastructure in hippocampus of model rats with Alzheimer's disease( AD). Methods Twenty-one male SD rats were equally divided into control,AD model and triptolide-treated groups. The AD model group were made with unilateral microinjection of aggregated beta-amyloid protein( Aβ)1 ~ 40 into hippocampus in rats and the control group rats were injected with normal saline in the same way. The triptolide-treated group rats were administered triptolide intraperitoneally after microinjection of aggregated Aβ1 ~ 40 into hippocampus. The i NOS expression and synaptic ultrastructure in hippocampus of each group were assayed by immunohistochemical staining and transmission electron microscope.Results Immunohistochemically,the cell number and average optical density of i NOS positive staining in the AD model group were higher than those of control group( P0. 01),the average optical density of i NOS positive staining in the triptolide-treated group were lower than that of AD model group( P0. 05). The number of synapses and synaptic vesicles and the thickness of postsynaptic density of hippocampal neuropil in the AD model group were lower than those of control group. The number of synapses and synaptic vesicles and the thickness of postsynaptic density of hippocampal neuropil in the triptolide-treated group were higher than those of AD model group. Conclusions Triptolide could inhibit i NOS expression and alleviate the degeneration of synapses in hippocampus of model rats with AD.
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Objective To explore the effects of triptolide on the expression of inducible nitric oxide synthase( i NOS) and synaptic ultrastructure in hippocampus of model rats with Alzheimer's disease( AD). Methods Twenty-one male SD rats were equally divided into control,AD model and triptolide-treated groups. The AD model group were made with unilateral microinjection of aggregated beta-amyloid protein( Aβ)1 ~ 40 into hippocampus in rats and the control group rats were injected with normal saline in the same way. The triptolide-treated group rats were administered triptolide intraperitoneally after microinjection of aggregated Aβ1 ~ 40 into hippocampus. The i NOS expression and synaptic ultrastructure in hippocampus of each group were assayed by immunohistochemical staining and transmission electron microscope.Results Immunohistochemically,the cell number and average optical density of i NOS positive staining in the AD model group were higher than those of control group( P0. 01),the average optical density of i NOS positive staining in the triptolide-treated group were lower than that of AD model group( P0. 05). The number of synapses and synaptic vesicles and the thickness of postsynaptic density of hippocampal neuropil in the AD model group were lower than those of control group. The number of synapses and synaptic vesicles and the thickness of postsynaptic density of hippocampal neuropil in the triptolide-treated group were higher than those of AD model group. Conclusions Triptolide could inhibit i NOS expression and alleviate the degeneration of synapses in hippocampus of model rats with AD.
Key concepts: Triptolide, Postsynaptic density, Neuropil, Hippocampus, Nitric oxide synthase, Hippocampal formation, Microinjection, Postsynaptic potential