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.
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.