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脑益康对D-半乳糖和亚硝酸钠诱导的阿尔茨海默病模型小鼠的保护作用

[Protective effect of Naoyikang on the Alzheimer's disease model mice induced by D-galactose and NaNO2].

作者信息

Zhu Yan, Zhou Ai-Ling, Mao Jia-Hui, Hu Ya-E, Shi Hai-Yan

机构信息

Department of Pathophysiology, School of Medical Sciences, Nantong University, Nantong 226001, China.

出版信息

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2008 Aug;24(3):296-300.

PMID:21141587
Abstract

AIM

To investigate the mechanisms of Naoyikang (Traditional Chinese Medicine) on the Alzheimer's Disease (AD) model mice induced by D-galactose (D-gal) and NaNO2.

METHODS

The mouse model was established by intraperitoneal injection of D-gal and NaNO2. The capacity of learning and memory was tested on mice with electrical maze; the content of nitric oxide (NO) and the activity of monoamine oxidase-B (MAO-B), glutathione peroxidase (GSH-PX), Na(+) -K(+) -ATP enzyme and Ca(2+) -ATP enzyme in cerebral cortex and hippocampus were assayed by biochemical methods; expression of Bax and Bcl-2 mRNA was detested by RT-PCR.

RESULTS

Naoyikang could ameliorate the capacity of learning and memory of AD model mice and reduce MAO-B activity in the brain tissue and activate the activity of Na(+) -K(+) -ATP enzyme and Ca(2+) -ATP enzyme in the brain tissue and decrease the expression of Bax mRNA, but increase the expression of Bcl-2 mRNA in the model brain tissue.

CONCLUSION

Naoyikang could protect AD model mice induced by D-gal and NaNO2. It could modify the metabolism of monoamine neurotransmitter in brain through reducing MAO-B activity and protect neurons by activating the activity of Na(+) -K(+) -ATP enzyme and Ca(2+) -ATP enzyme and decrease Bax expression and increase Bcl-2 expression in the model brain tissue.

摘要

目的

探讨脑益康(中药)对D-半乳糖(D-gal)和亚硝酸钠诱导的阿尔茨海默病(AD)模型小鼠的作用机制。

方法

通过腹腔注射D-半乳糖和亚硝酸钠建立小鼠模型。用电迷宫测试小鼠的学习记忆能力;采用生化方法检测大脑皮质和海马中一氧化氮(NO)含量、单胺氧化酶B(MAO-B)、谷胱甘肽过氧化物酶(GSH-PX)、钠钾ATP酶(Na(+) -K(+) -ATP酶)和钙ATP酶(Ca(2+) -ATP酶)的活性;用逆转录聚合酶链反应(RT-PCR)检测Bax和Bcl-2 mRNA的表达。

结果

脑益康可改善AD模型小鼠的学习记忆能力,降低脑组织中MAO-B活性,激活脑组织中Na(+) -K(+) -ATP酶和Ca(2+) -ATP酶的活性,降低模型脑组织中Bax mRNA的表达,但增加Bcl-2 mRNA的表达。

结论

脑益康对D-半乳糖和亚硝酸钠诱导的AD模型小鼠具有保护作用。它可通过降低MAO-B活性来调节脑内单胺类神经递质的代谢,通过激活Na(+) -K(+) -ATP酶和Ca(2+) -ATP酶的活性保护神经元,并降低模型脑组织中Bax的表达,增加Bcl-2的表达。

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