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Research ArticleOriginal Article
Open Access

Berberine and total base from rhizoma coptis chinensis attenuate brain injury in an aluminum-induced rat model of neurodegenerative disease

Jingo Zhang, Jun Qing Yang, Bai Cheng He, Qi Xin Zhou, Hua Rong Yu, Yong Tang and Bei Zhong Liu
Saudi Medical Journal June 2009, 30 (6) 760-766;
Jingo Zhang
Department of Pharmacology, Chongqing Medical University, Chongqing, China.
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Jun Qing Yang
Department of Pharmacology, Chongqing Medical University, Chongqing, China.
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Bai Cheng He
Department of Pharmacology, Chongqing Medical University, Chongqing, China.
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Qi Xin Zhou
Department of Pharmacology, Chongqing Medical University, Chongqing, China.
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Hua Rong Yu
Department of Pharmacology, Chongqing Medical University, Chongqing, China.
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Yong Tang
Department of Pharmacology, Chongqing Medical University, Chongqing, China.
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Bei Zhong Liu
Department of Pharmacology, Chongqing Medical University, Chongqing, China.
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Abstract

OBJECTIVE: To investigate the protective effects of the total base from rhizoma coptis chinensis (CTB) and berberine (Ber) on neurodegeneration induced by aluminum overload in rats.

METHODS: The study took place in the Department of Pharmacology, Chongqing Medical University, Chongqing, China, between February 2005 and May 2007. Wistar rats were divided into control group, model group, Ber-treated group, CTB (55 mg/kg and 110 mg/kg)-treated group, and nimodipine-treated group (n=20). A rat brain damage model was established via intragastric administration of 400 mg/kg element aluminum once a day, 5 days a week for 12 weeks. The CTB, Ber, and nimodipine were intragastrically administered 4 hours after each aluminum administration for 12 weeks. The morphological changes of the neurons of the rat hippocampus and the changes of rat learning and memory functions were observed. The superoxide dismutase (SOD), choline acetyltransferase (ChAT), acetylcholinesterase (AchE), and monoamine oxidase-B (MAO-B) activities and malondialdehyde (MDA) content, as well as the MAO-B expression in the rat brain were examined.

RESULTS: The CTB, Ber, and nimodipine significantly improved the learning and memory ability impairment and hippocampal neuronal death. The CTB, Ber, and nimodipine also significantly blunted the decrease of SOD and ChAT activities, and the increase of MDA content, AchE activities, and MAO-B expressions and activity in the aluminum-overload rats.

CONCLUSION: The CTB and Ber have protective effects on neurodegeneration induced by aluminum overload. The CTB (110 mg/kg) has more powerful neuroprotection than Ber. The CTB and Ber have protective effects on neurodegeneration induced by aluminum overload. The CTB (110 mg/kg) has more powerful neuroprotection than Ber.

  • Copyright: © Saudi Medical Journal

This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Saudi Medical Journal: 30 (6)
Saudi Medical Journal
Vol. 30, Issue 6
1 Jun 2009
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Berberine and total base from rhizoma coptis chinensis attenuate brain injury in an aluminum-induced rat model of neurodegenerative disease
Jingo Zhang, Jun Qing Yang, Bai Cheng He, Qi Xin Zhou, Hua Rong Yu, Yong Tang, Bei Zhong Liu
Saudi Medical Journal Jun 2009, 30 (6) 760-766;

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Berberine and total base from rhizoma coptis chinensis attenuate brain injury in an aluminum-induced rat model of neurodegenerative disease
Jingo Zhang, Jun Qing Yang, Bai Cheng He, Qi Xin Zhou, Hua Rong Yu, Yong Tang, Bei Zhong Liu
Saudi Medical Journal Jun 2009, 30 (6) 760-766;
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© 2025 Saudi Medical Journal Saudi Medical Journal is copyright under the Berne Convention and the International Copyright Convention.  Saudi Medical Journal is an Open Access journal and articles published are distributed under the terms of the Creative Commons Attribution-NonCommercial License (CC BY-NC). Readers may copy, distribute, and display the work for non-commercial purposes with the proper citation of the original work. Electronic ISSN 1658-3175. Print ISSN 0379-5284.

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