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The Effect of 3′,4′-Dihydroxyflavonol on Lipid Peroxidation in Rats with Cerebral Ischemia Reperfusion Injury

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Abstract

The aim of present study was to determine the effect of 3′,4′-dihydroxyflavonol (DiOHF) on lipid peroxidation in experimental brain ischemia–reperfusion in rats. Present study was performed on the 34 male Wistar-albino rats, weigth 350-400 g. Experiment groups were designed as 1-Sham; 2-Ischemia–reperfusion; animal were anesthesized and carotid arteried were clemped for 20 min and reperfusion (7 days). 3-DiOHF + Ischemia–reperfusion; DiOHF was given to animals as 10 mg/kg by intraperitoneal. 4- Ischemia + DiOHF + Reperfusion; 5- Ischemia–reperfusion + DiOHF. Blood samples and serebral cortex were analysed for malondyaldehyde (MDA), NO (nitric oxide), xanthine oxidase (XO), glutathione (GSH) and glutathione peroxidase (GPx). Blood MDA levels were significantly higher ischemia–reperfusion groups (P < 0.005). However, DiOHF inhibited MDA. Ischemia–reperfusion led to increased XO and NO but DiOHF supplementation reduced NO and XO. DiOHF increased GSH and GPx levels compared to ischemia–reperfusion group. All together, our present study showed that intraperitoneal DiOHF supplementation has protective effect on brain ischaemia–reperfusion injury in rat.

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Acknowledgments

This study was supported by a grant Selcuk University, Scientific Research Council (Grant Number is 14202015).

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Authors and Affiliations

  1. Department of Physiology, Faculty of Medicine, Selcuk University, Konya, Turkey

    Merve Caliskan, Rasim Mogulkoc & Abdulkerim Kasim Baltaci

  2. Department of Biochemistry, Faculty of Medicine, Selcuk University, Konya, Turkey

    Esma Menevse

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  1. Merve Caliskan
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  2. Rasim Mogulkoc
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Correspondence to Rasim Mogulkoc.

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Caliskan, M., Mogulkoc, R., Baltaci, A.K. et al. The Effect of 3′,4′-Dihydroxyflavonol on Lipid Peroxidation in Rats with Cerebral Ischemia Reperfusion Injury. Neurochem Res 41, 1732–1740 (2016). https://doi.org/10.1007/s11064-016-1889-x

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  • DOI: https://doi.org/10.1007/s11064-016-1889-x

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