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Published on: May 23, 2011
Effect of 3',4'-Dihydroxyflavonol on Cortex Oxidant/Antioxidant System and Transmitter Levels in Brain
Lemanur Soysal1, Ebru Kubra Uzdil1, Tugce Aladag1
1Selcuk University, Medical School, Department of Physiology, Konya, Turkey.
Introduction:
Survivors of global cerebral ischemia (GCI) are at a high risk of developing neurological disorders. Cerebral infarction resulting from GCI may lead to neuronal loss and subsequent brain damage. In the present study, we investigated the effect of one-week 3',4'- Dihydroxyflavonol (DiOHF) supplementation on the oxidant-antioxidant system and neurotransmitter levels in the cerebral cortex of rats subjected to brain ischemia-reperfusion.
Methods:
The study was performed on male Wistar albino rats. A total of 28 rats were used in the study, and the groups were formed as follows. Control Group (n=6): No anesthesia or surgical procedure was performed on the animals in this group. Sham Group (n=6): After general anesthesia was induced in the animals in this group, the carotid artery regions were opened and closed. After the application, the vehicle application was performed for 1 week (1 ml DiOHF vehicle). Ischemia- Reperfusion (I/R) Group (n=8): After the carotid arteries were isolated in the rats under general anesthesia, they were ligated for 30 minutes, and ischemia was performed, followed by reperfusion. Following reperfusion, 1 ml of DiOHF vehicle was supplemented for 1 week. Ischemia-Reperfusion Group + DiOHF Supplemented (n=8): After the carotid arteries were isolated in rats under general anesthesia, they were ligated for 30 minutes, followed by ischemia and reperfusion. Subsequently, DiOHF supplementation was performed for 1 week.
Results:
Experimental cerebral ischemia-reperfusion in rats caused a significant increase in malondialdehyde (MDA) levels, a marker of oxidative stress, in the cerebral cortex, while markedly decreasing antioxidant enzymes such as GPx, SOD, CAT, and Trx2. Additionally, cerebral I/R elevated the levels of neurotransmitters glutamate and GABA. However, one week of DiOHF supplementation following ischemia-reperfusion ameliorated these alterations in the frontal cortex tissue.
Discussion:
Overall, the findings showed that DiOHF administration for one week after experimental cerebral ischemia-reperfusion in rats exerts beneficial effects on the oxidant/antioxidant system and neurotransmitter levels in frontal cortex tissue.
Conclusion:
This study showed that by lowering oxidative stress and restoring neurotransmitter levels in the frontal cortex, a one-week treatment with 3',4'-Dihydroxyflavonol after cerebral ischemia- reperfusion in rats has protective benefits. Following an ischemic stroke, DiOHF may be a viable treatment for reducing neuronal damage.
