Abstract
In this study, we investigated the neuroprotective effects of paclitaxel in transient cerebral ischemia and possible regulatory mechanism of these neuroprotection. Our data showed that paclitaxel can down-regulate the increased MLK3, JNK3, c-Jun, Bcl-2, and caspase-3 phosphorylation induced by ischemia injury. Cresyl violet staining and immunohistochemistry results demonstrated that paclitaxel had neuroprotective effect against ischemia/reperfusion-induced neuronal cell death. These results indicated that paclitaxel has neuroprotection in ischemic injury through JNK3 signaling pathway and provided a novel possible drug in therapeutics of brain ischemia.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antineoplastic Agents, Phytogenic / pharmacology*
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Brain Ischemia / enzymology*
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Caspase 3 / metabolism
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Cell Death
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Humans
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JNK Mitogen-Activated Protein Kinases / metabolism
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MAP Kinase Kinase Kinases / metabolism
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MAP Kinase Signaling System / drug effects
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Male
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Mitogen-Activated Protein Kinase 10 / metabolism*
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Mitogen-Activated Protein Kinase Kinase Kinase 11
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Neurons / drug effects
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Neurons / enzymology
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Neuroprotective Agents / pharmacology*
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Paclitaxel / pharmacology*
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Phosphorylation / drug effects
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Rats
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Rats, Sprague-Dawley
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Reperfusion Injury / enzymology*
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Tubulin Modulators / pharmacology*
Substances
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Antineoplastic Agents, Phytogenic
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Neuroprotective Agents
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Tubulin Modulators
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Mitogen-Activated Protein Kinase 10
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JNK Mitogen-Activated Protein Kinases
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MAP Kinase Kinase Kinases
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Caspase 3
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Paclitaxel