ABSTRACT
Objective To investigate the effect of CYP46A1 on the pathogenesis of Alzheimer's disease.Methods Recombinant lentiviral vectors which including anthropogenic CYP46A1 were injected into bilateral hippocampus of 3-monthold male 5XFAD transgenic mice,while empty vectors were injected into the corresponding position of the control group.After two months,the ability of learning and memory were tested by Morris water maze and T maze experiments,and amyloid plaque and inflammatory infiltration in the brain were detected by immunohistochemical staining and ELISA respectively.Results Compared with the control group,CYP46A1 virus injection significantly increased the CYP46A1 mRNA and protein expression in hippocampus.In addition,CYP46A1 overexpression significantly decreased the latency to find the platform in Morris water maze test and increased the correct rate to choose in T maze test.Aβ immunohistochemical staining and plaques area statistics demonstrated that the amyloid plaque area of hippocampus in CYP46A1 overexpression mice was significantly reduced,and there was a significantly decrease of hippocampal astrocytes expression by means of GFAP staining.Furthermore,hippocampal CYP46A1 overexpression significantly decreased the expression level of Aβ40,Aβ42,IL-1β and TNF-α,while compare with the control group.Conclusion CYP46A1 overexpression in hippocampus can promote the cognitive impairment,as well as ameliorate the brain inflammatory infiltration in 5XFAD transgenic mice,suggesting that CYP46A1 has anti-Alzheimer's disease like effects.
ABSTRACT
Objective To explore effect of early moxibustion intervention on cerebral Aβ1-40 in a mouse model of Alzheimer disease (AD) and the mechanism of action of moxibusion in preventing and treating AD.Method Gene phenotype in transgenic AD passage mice was identified using PCR. One and a half-month-old female Tg6799 transgenic mice were randomly allocated, including nine mice to a model group and eight mice to a treatment group. Nine C57BL/6J wild type female mice of the same age and background constituted a normal control group. Wheat-grain-sized moxa cone moxibustion on bilateral points Xinshu(BL15) and Shenshu(BL23) was given to the treatment group. After the completion of treatment, Aβ1-40 expression in mouse frontal cortex and hippocampal region was determined using the immunohistochemical method.Result Aβ1-40 expression in mouse frontal cortex and hippocampal region decreased significantly in the treatment group compared with the model group (P<0.01,P<0.05). Conclusion Early moxibustion intervention can decrease cerebral Aβ1-40 expression and delay AD pathological process in a mouse model of AD.
ABSTRACT
Objective To explore effect of early moxibustion intervention on cerebral Aβ1-40 in a mouse model of Alzheimer disease (AD) and the mechanism of action of moxibusion in preventing and treating AD.Method Gene phenotype in transgenic AD passage mice was identified using PCR. One and a half-month-old female Tg6799 transgenic mice were randomly allocated, including nine mice to a model group and eight mice to a treatment group. Nine C57BL/6J wild type female mice of the same age and background constituted a normal control group. Wheat-grain-sized moxa cone moxibustion on bilateral points Xinshu(BL15) and Shenshu(BL23) was given to the treatment group. After the completion of treatment, Aβ1-40 expression in mouse frontal cortex and hippocampal region was determined using the immunohistochemical method.Result Aβ1-40 expression in mouse frontal cortex and hippocampal region decreased significantly in the treatment group compared with the model group (P<0.01,P<0.05). Conclusion Early moxibustion intervention can decrease cerebral Aβ1-40 expression and delay AD pathological process in a mouse model of AD.
ABSTRACT
Objective To study the effects ofShenqi YizhiGranules (SQYZ) on learning and memory and content of Aβ1-42 of cerebral tissue in 5XFAD mice with Alzheimer’s disease; To discuss its mechanism on improving learning and memory ability of 5XFAD mice.Methods Four-month-old C57BL?6 wild type mice were randomly divided into NS control group and SQYZ control group, and the 5XFAD mice were randomly divided into model group, SQYZ group and huperzine-A (HupA) group, 15 mice in each group. Each group were given same volume for gavage for 60 d. After treatment, the learning and memory ability were evaluated by nesting test, passive avoidance and Morris water maze test. The senile plaques and content of Aβ1-42, ionized calcium binding adapter molecule 1 and glial fibrillary acidic protein in cerebral cortex and hippocampus were detected by immunohistochemical staining and immunofluorescence, respectively.Results Compared with NS control group, the score of nesting test in model group significantly decreased; the step-through latency in passive avoidance was shortened and the escape latentcy in Morris water maze test was prolonged; the quantity of senile plaques and content of Aβ1-42 increased in cerebral cortex and hippocampus; the activation of glial cells significantly increased. In the SQYZ group, the above-mentioned indexes reached or approached the level of wild type control mice. The difference between SQYZ group and model group was statistically significant (P<0.05,P<0.01).Conclusion SQYZ improved learning and memory ability in 5XFAD mice, which may be related to reduction of senile plaques, inhibition of over activation in glial cells and reduction of content of Aβ1-42 in cerebral cortex and hippocampus.