Journal of vascular surgery · 2007
Resveratrol neuroprotective effects during focal cerebral ischemia injury via nitric oxide mechanism in rats.
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Tsai Shen-Kou, Hung Li-Man, Fu Yuan-Tsung, Cheng Henrich, Nien Mao-Wei, Liu Hsin-Yi, Zhang Friedrich Bo-Yuan, Huang Shiang-Suo
Аннотация
BACKGROUND: Our prior study showed that resveratrol could suppress infarct volume and exert neuroprotective effect on rats subjected to focal cerebral ischemia (FCI) injury. Recently, it has been reported in some literature that resveratrol protects the spinal cord, kidney, and heart from ischemia-reperfusion injury through upregulation of nitric oxide (NO). Therefore, this study was designed to investigate the role of nitric oxide on the neuroprotective mechanisms of resveratrol on rats after FCI injury.
METHODS: The FCI injury was induced by the middle cerebral artery (MCA) occlusion for 1 hour and then a 24-hour reperfusion followed in the anesthetized Long-Evans rats. Resveratrol was intravenously injected after 1 hour MCA occlusion.
RESULTS: Treatment of resveratrol (0.1 and 1 microg/kg) decreased the lactate dehydrogenase (LDH) in plasma and malondialdehyde (MDA) in FCI injury brain tissue, whereas the level of NO in plasma was increased. In addition, resveratrol downregulated protein and mRNA expression of inducible nitric oxide synthase (iNOS), and upregulated protein and mRNA expression of endothelial nitric oxide synthase (eNOS), while the expression of protein and mRNA of neuronal nitric oxide synthase (nNOS) was unchanged. Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME, the nonselective NOS inhibitor) or L-N(5)-(1-iminoethyl)-ornithine (L-NIO, the eNOS selective inhibitor) completely blocked the effect of resveratrol in decreasing infarction volumes.
CONCLUSIONS: This study demonstrated the important role of NO in the neuroprotective effect of resveratrol in FCI injury.
METHODS: The FCI injury was induced by the middle cerebral artery (MCA) occlusion for 1 hour and then a 24-hour reperfusion followed in the anesthetized Long-Evans rats. Resveratrol was intravenously injected after 1 hour MCA occlusion.
RESULTS: Treatment of resveratrol (0.1 and 1 microg/kg) decreased the lactate dehydrogenase (LDH) in plasma and malondialdehyde (MDA) in FCI injury brain tissue, whereas the level of NO in plasma was increased. In addition, resveratrol downregulated protein and mRNA expression of inducible nitric oxide synthase (iNOS), and upregulated protein and mRNA expression of endothelial nitric oxide synthase (eNOS), while the expression of protein and mRNA of neuronal nitric oxide synthase (nNOS) was unchanged. Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME, the nonselective NOS inhibitor) or L-N(5)-(1-iminoethyl)-ornithine (L-NIO, the eNOS selective inhibitor) completely blocked the effect of resveratrol in decreasing infarction volumes.
CONCLUSIONS: This study demonstrated the important role of NO in the neuroprotective effect of resveratrol in FCI injury.
Предметные рубрики MeSH
AnimalsBrainBrain IschemiaCarotid ArteriesDisease Models, AnimalDose-Response Relationship, DrugEnzyme InhibitorsInfarction, Middle Cerebral ArteryL-Lactate DehydrogenaseLigationMaleMalondialdehydeMiddle Cerebral ArteryNG-Nitroarginine Methyl EsterNeuroprotective AgentsNitric OxideNitric Oxide SynthaseOrnithineRNA, MessengerRatsRats, Long-EvansResveratrolStilbenesUp-Regulation