Abstract | AIM: METHODS: RESULTS:
Caffeic acid (50 mg/kg) ameliorated neurological dysfunction and neuron loss, and decreased infarct volume 24 h after ischemia; it attenuated brain atrophy, infarct volume, and particularly astrocyte proliferation 14 d after ischemia. In addition, it reduced the production of leukotrienes (5-lipoxygenase metabolites) in the ischemic hemispheres 3 h and 7 d after ischemia. CONCLUSION:
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Authors | Yu Zhou, San-hua Fang, Yi-lu Ye, Li-sheng Chu, Wei-ping Zhang, Meng-ling Wang, Er-qing Wei |
Journal | Acta pharmacologica Sinica
(Acta Pharmacol Sin)
Vol. 27
Issue 9
Pg. 1103-10
(Sep 2006)
ISSN: 1671-4083 [Print] United States |
PMID | 16923329
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antioxidants
- Caffeic Acids
- Leukotrienes
- Neuroprotective Agents
- cysteinyl-leukotriene
- Leukotriene B4
- Arachidonate 5-Lipoxygenase
- Cysteine
- caffeic acid
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Topics |
- Animals
- Antioxidants
(pharmacology)
- Arachidonate 5-Lipoxygenase
(metabolism)
- Brain
(pathology)
- Caffeic Acids
(pharmacology)
- Cysteine
(metabolism)
- Infarction, Middle Cerebral Artery
(complications)
- Ischemic Attack, Transient
(etiology, metabolism, pathology)
- Leukotriene B4
(metabolism)
- Leukotrienes
(metabolism)
- Male
- Neurons
(drug effects)
- Neuroprotective Agents
(pharmacology)
- Rats
- Rats, Sprague-Dawley
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