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小檗碱对三转基因阿尔茨海默病小鼠海马组织Aβ和Bcl-2、Bax表达的影响 被引量:4

Effects of Berberine on the Expression of Amyloid-β and Bax,Bcl-2 in Hippocampus of Three Transgenic Mice with Alzheimer's disease
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摘要 目的:观察旋小檗碱对APP/PS1/Tau三转基因阿尔茨海默病(AD)小鼠海马组织β-淀粉样蛋白(Aβ)和Bcl-2、Bax表达的影响。方法:20只三转基因AD小鼠随机分为对照组和给药组,各10只。加药组给予小檗碱50 mg·kg^(-1)·d^(-1)灌胃,对照组给予等容量生理盐水灌胃,共3个月。Western Blot检测小鼠海马组织蛋白Aβ、Bcl-2和Bax表达,免疫组化测定小鼠海马Aβ表达,ELISA检测小鼠海马Bcl-2、Bax表达。结果:给药组海马组织Aβ表达较对照组降低(P<0.05);与对照组比较,给药组海马组织Bcl-2表达增加而Bax表达减少(P<0.05)。结论:小檗碱能降低三转基因AD小鼠的Aβ表达,其机制可能与Bcl-2和Bax表达改变有关。 Objective: To observe the effect ofberberine on the expression of amyloid-β (Aβ), Bcl-2 and Bax in the hippocampus ofAPP/PS1/Tau threetransgenic mice ofAlzheimer' s disease (AD). Methods: Twenty APP/ PS1/Tau three transgenic AD (3XTg-AD) mice were randomly divided into control group and treatment group (n=10 respectively). Mice in treatment group were treated with berberine at the dose of 50 mg·kg^-1· d^-1 by gastric gavage orally for 90 days. Mice in control group were treated with the normal saline at the same dose by gasteic garage orally for 90 days. The Aβ, Bcl-2 and Bax protein in hippocampus were detected by western blot. The ex- pression of Aβ in the hippocampus was determined by immunohistochemistry. The Bcl-2 and Bax protein in hip- pocampus was detected by ELISA. Results: Compared with the control group, the expression of Aβ in the hip- pocampus of the berberine group was significantly decreased (P〈0.05); the expression of Bcl-2 was more inten- sive in hippocampus tissue of berberine group than that of control group (P〈0.05), but the expression of Bax was the opposite (P〈0.05). Conclusion: Berberine can decrease the expression of Aβ in the hippocampus of APP/ PS 1/Tau three transgenic AD mice, and up-regulating Bcl-2 expression and down-regulating Bax expression may play a role in the mechanism.
出处 《神经损伤与功能重建》 2017年第3期194-196,共3页 Neural Injury and Functional Reconstruction
基金 深圳市科技研发资金项目(No.JCYJ20150529112551484)
关键词 阿尔茨海默病 小檗碱 三转基因小鼠 Β-淀粉样蛋白 凋亡 Alzheimer' s disease berberine three transganic mice amyloid-β apoptosis
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