Abstract
Berberine (BBR), one of the major constituents of Chinese herb Rhizoma coptidis, has been reported to exert beneficial effects to various diseases, including Alzheimer's disease (AD). In the present work, we aimed to investigate the effects of BBR on neuronal cell death induced by homocysteic acid (HCA), which was considered as a risk of AD. BBR significantly reduced HCA-induced reactive oxygen species (ROS) generation, lactate dehydrogenase release and subsequent cell death. LY294002, the PI3K inhibitor, blocked the protection as well as the up-regulation of Akt phosphorylation of BBR. Taken together, our results indicate that BBR protects HCA-induced HT-22 cell death partly via modulating Akt pathway, suggesting BBR may be a promising therapeutic agent for the treatment of HCA-related diseases, including AD.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis / drug effects
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Berberine / therapeutic use*
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Cell Line
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Chromones / pharmacology
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Drug Evaluation, Preclinical
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Homocysteine / analogs & derivatives*
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Homocysteine / toxicity
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Membrane Potential, Mitochondrial / drug effects
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Mice
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Morpholines / pharmacology
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Nerve Tissue Proteins / physiology*
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Neurons / drug effects*
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Neurons / metabolism
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Phosphoinositide-3 Kinase Inhibitors
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Phosphorylation / drug effects
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Protein Processing, Post-Translational / drug effects
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Proto-Oncogene Proteins c-akt / physiology*
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Reactive Oxygen Species / metabolism
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Signal Transduction / drug effects*
Substances
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Chromones
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Morpholines
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Nerve Tissue Proteins
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Phosphoinositide-3 Kinase Inhibitors
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Reactive Oxygen Species
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Berberine
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Homocysteine
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homocysteic acid
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2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
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Akt1 protein, mouse
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Proto-Oncogene Proteins c-akt