Abstract
The purpose of this study was to determine whether the Laurus nobilis chloroform fraction (LNCF) protects against cerebral ischemia neuronal damage. Human neuroblastoma SH-SY5Y cells and brain slices from rats were subjected to oxygen and glucose deprivation (OGD), followed by reoxgenation with and without LNCF. The viabilities of SH-SY5Y cells and brain slices from the rats were 58.5±4.9% and 79.7±5.9% in the group subjected to OGD, and 80.4±0.4% and 97.2±1.9% at 4 µg/ml of LNCF, respectively. LNCF also significantly inhibited death-associated protein kinase (DAPK) dephosphorylation. Pretreatment with LNCF at 4 mg/kg significantly decreased infarct size by 79% of vehicle control in the middle cerebral artery occlusion (MCAO) in vivo model. LNCF is a neuroprotective drug candidate against cerebral ischemia neuronal damage.
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 Regulatory Proteins / metabolism
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Brain Infarction / metabolism
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Brain Infarction / pathology
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Brain Infarction / prevention & control
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Calcium-Calmodulin-Dependent Protein Kinases / metabolism
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Cell Death / drug effects*
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Cell Line, Tumor
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Cell Survival / drug effects
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Chloroform / chemistry*
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Death-Associated Protein Kinases
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Enzyme Activation / drug effects
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Gene Expression Regulation, Enzymologic / drug effects
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Glucose / deficiency*
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Hippocampus / drug effects
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Hippocampus / metabolism
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Hippocampus / pathology
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Humans
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Laurus / chemistry*
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Male
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Neurons / drug effects*
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Neurons / metabolism
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Neurons / pathology
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Neuroprotective Agents / isolation & purification
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Neuroprotective Agents / pharmacology
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Oxygen / metabolism*
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Phosphoproteins / metabolism
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Plant Extracts / isolation & purification
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Plant Extracts / pharmacology*
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Rats
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Rats, Sprague-Dawley
Substances
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Apoptosis Regulatory Proteins
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Neuroprotective Agents
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Phosphoproteins
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Plant Extracts
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Chloroform
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Death-Associated Protein Kinases
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Calcium-Calmodulin-Dependent Protein Kinases
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Glucose
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Oxygen