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Войти в исследования Journal of Alzheimer's disease reports · 2025
Protective effect of chlorogenic acid on cognitive impairment in rats with early Alzheimer's disease via Wnt signaling pathway.
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Wang Lei, Wang Xuehua, Hou Liang, Liu Yingxue, Liu Jiangsheng, Zhang Deqiang, Yao Suyan, Zheng Deyu
Аннотация
BACKGROUND: Chlorogenic acid (CGA) has neuroprotective properties associated with Alzheimer's disease (AD). However, the exact mechanism by which CGA prevents cognitive impairment in AD remains unclear. The purpose of this study was to investigate the protective effect of CGA on cognitive impairment in rats with early AD via the Wnt signaling pathway.
OBJECTIVE: To investigate the protective effect of CGA on cognitive impairment in an early AD rat model via the Wnt signaling pathway.
METHODS: Forty male rats were randomly divided into the control group (CON), AD group (AD), CGA 100 groups and CGA 150 groups with 10 rats in each group. In addition to CON group, the other three groups of rats were injected with 10 μL Aβ25-35 in the unilateral ventricle to create the model. After 3 days of molding, CGA100 group (gavage of CGA at a dose of 150 mg/kg/d) and CGA150 group (gavage of CGA at a dose of 150 mg/kg/d) were given CGA for 6 weeks. Morris water maze test, Nissl staining test, and western blot test were used.
RESULTS: CGA reduced the escape latency of Aβ25-35-induced early AD rats, shortened the swimming distance, and extended the activity time of the target quadrant. CGA increased the number of Nissl, decreased the expression of inflammatory factors, decreased the expression levels of GSK-3β, GFAP, and tau, and increased the expression levels of DVL2 and β-catenin.
CONCLUSIONS: CGA can protect the cognitive impairment of early AD rats via Wnt signaling pathway.
OBJECTIVE: To investigate the protective effect of CGA on cognitive impairment in an early AD rat model via the Wnt signaling pathway.
METHODS: Forty male rats were randomly divided into the control group (CON), AD group (AD), CGA 100 groups and CGA 150 groups with 10 rats in each group. In addition to CON group, the other three groups of rats were injected with 10 μL Aβ25-35 in the unilateral ventricle to create the model. After 3 days of molding, CGA100 group (gavage of CGA at a dose of 150 mg/kg/d) and CGA150 group (gavage of CGA at a dose of 150 mg/kg/d) were given CGA for 6 weeks. Morris water maze test, Nissl staining test, and western blot test were used.
RESULTS: CGA reduced the escape latency of Aβ25-35-induced early AD rats, shortened the swimming distance, and extended the activity time of the target quadrant. CGA increased the number of Nissl, decreased the expression of inflammatory factors, decreased the expression levels of GSK-3β, GFAP, and tau, and increased the expression levels of DVL2 and β-catenin.
CONCLUSIONS: CGA can protect the cognitive impairment of early AD rats via Wnt signaling pathway.