Many studies of brain ischemia have shown the role played by massive ischemia-induced production of reactive oxygen species, the main mechanism of neuronal death. However, currently, there is no treatment choice to prevent cell death triggered by reactive oxygen species. In our study, we researched the effects of tannic acid, an antioxidant, on the ischemic tissue of rats with induced middle cerebral artery occlusion. The animals were divided into three groups of eight animals. The sham group were only administered 10 % ethanol intraperitoneally, the second group had middle cerebral artery occlusion induced and were given 10 % ethanol intraperitoneally, while the third group had middle cerebral artery occlusion with 10 mg/kg dose tannic acid dissolved in 10 % ethanol administered within half an hour intraperitoneally. The rats were sacrificed 24 h later, and brain tissue was examined biochemically and histopathologically. Biochemical evaluation of brain tissue found that comparing the ischemic group with no treatment with the tannic acid-treated ischemia group; the superoxide dismutase (SOD) levels were higher, malondialdehyde (MDA) levels were lower, and nuclear respiratory factor-1 (NRF-1) was higher in the tannic acid-treated group. Histopathological examination showed that the histopathological results of the tannic acid group were better than the group not given tannic acid. Biochemical and histopathological results showed that tannic acid administration had an antioxidant effect on the negative effects of ischemia in brain tissue.
antioxidants cerebrum ischemia tannic acid
This is a preview of subscription content, log in to check access.
This study was supported by the Canakkale Onsekiz Mart University Experimental Research Center (COMUDAM).
Conflict of Interest
The authors declare no conflicts of interest.
No financial support.
Rosamond, W., K. Flegal, G. Friday, et al. 2007. Heart disease and stroke statistics—2007 update: A report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 115: 69–171.CrossRefGoogle Scholar
Lloyd-Jones, D., R.J. Adams, T.M. Brown, et al. 2010. Executive summary: heart disease and stroke statistics—2010 update: A report from the American Heart Association. Circulation 121: 948–954.PubMedCrossRefGoogle Scholar
Marler, J., T. Brott, J. Broderick, et al. 1995. Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. New England Journal of Medicine 333: 1581–1587.CrossRefGoogle Scholar
Moro, M.A., A. Almeida, J.P. Bolanos, and I. Lizasoain. 2005. Mitochondrial respiratory chain and free radical generation in stroke. Free Radical Biology and Medicine 39: 1291–1304.PubMedCrossRefGoogle Scholar
Chan, P.H. 2001. Reactive oxygen radicals in signaling and damage in the ischemic brain. Journal of Cerebral Blood Flow and Metabolism 21: 2–14.PubMedCrossRefGoogle Scholar
Giulivi, C., A. Boveris, and E. Cadenas. 1995. Hydroxyl radical generation during mitochondrial electron transfer and the formation of 8-hydroxydesoxyguanosine in mitochondrial DNA. Archives of Biochemistry and Biophysics 316: 909–916.PubMedCrossRefGoogle Scholar
Khan, N.S., A. Ahmad, and S.M. Hadi. 2000. Anti-oxidant, pro-oxidant properties of tannic acid and its binding to DNA. Chemico-Biological Interactions 125: 177–189.PubMedCrossRefGoogle Scholar
Chang, T.L., and C.H. Wang. 2013. Combination of quercetin and tannic acid in inhibiting 26S proteasome affects S5a and 20S expression, and accumulation of ubiquitin resulted in apoptosis in cancer chemoprevention. Biological Chemistry 394: 561–575.PubMedCrossRefGoogle Scholar
Buzzini, P., P. Arapitsas, M. Goretti, et al. 2008. Antimicrobial and antiviral activity of hydrolysable tannins. Mini Reviews in Medicinal Chemistry 8: 1179–1187.PubMedCrossRefGoogle Scholar
Winiarska-Mieczan, A., R. Krusinski, and M. Kwiecien. 2013. Tannic acid influence on lead and cadmium accumulation in the hearts and lungs of rats. Advances in Clinical and Experimental Medicine 22: 615–620.PubMedGoogle Scholar
Kraus, T.E., R.A. Dahlgren, and R.J. Zasoski. 2003. Tannins in nutrient dynamics of forest ecosystems—A review. Plant and Soil 256: 41–66.CrossRefGoogle Scholar
Gülįin, I., Z. Huyut, M. Elmastas, and H. Aboul-Enein. 2010. Radical scavenging and antioxidant activity of tannic acid. Arabian Journal of Chemistry 3: 43–53.CrossRefGoogle Scholar
Sánchez-Moreno, C., A. Jiménez-Escrig, and F. Saura-Calixto. 2000. Study of low-density lipoprotein oxidizability indexes to measure the antioxidant activity of dietary polyphenols. Nutrition Research 20: 941–953.CrossRefGoogle Scholar
Longa, E.Z., P.R. Weinstein, S. Carlson, and R. Cummins. 1989. Reversible middle cerebral artery occlusion without craniectomy in rats. Stroke 20: 84–91.PubMedCrossRefGoogle Scholar
Mansoorali, K.P., T. Prakash, D. Kotresha, K. Prabhu, and N. Rama Rao. 2012. Cerebroprotective effect of Eclipta alba against global model of cerebral ischemia induced oxidative stress in rats. Phytomedicine: International Journal of Phytotherapy and Phytopharmacology 19: 1108–1116.CrossRefGoogle Scholar
Kumar, M.H., and Y.K. Gupta. 2002. Antioxidant property of Celastrus paniculatus willd: A possible mechanism in enhancing cognition. Phytomedicine : International Journal of Phytotherapy and Phytopharmacology 9: 302–311.CrossRefGoogle Scholar
Kirisattayakul, W., J. Wattanathorn, T. Tong-Un, et al. 2013. Cerebroprotective effect of Moringa oleifera against focal ischemic stroke induced by middle cerebral artery occlusion. Oxidative Medicine and Cellular Longevity 2013: 1–10.CrossRefGoogle Scholar
Viswanatha, G.L., H. Shylaja, and C.G. Mohan. 2013. Alleviation of transient global ischemia/reperfusion-induced brain injury in rats with 1,2,3,4,6-penta-O-galloyl-beta-d-glucopyranose isolated from Mangifera indica. European Journal of Pharmacology 720: 286–293.PubMedCrossRefGoogle Scholar
Mandemakers, W., V.A. Morais, and B. De Strooper. 2007. A cell biological perspective on mitochondrial dysfunction in Parkinson disease and other neurodegenerative diseases. Journal of Cell Science 120: 1707–1716.PubMedCrossRefGoogle Scholar
Valerio, A., P. Bertolotti, A. Delbarba, et al. 2011. Glycogen synthase kinase-3 inhibition reduces ischemic cerebral damage, restores impaired mitochondrial biogenesis and prevents ROS production. Journal of Neurochemistry 116: 1148–1159.PubMedCrossRefGoogle Scholar
Zhang, Q., Y. Wu, H. Sha, et al. 2012. Early exercise affects mitochondrial transcription factors expression after cerebral ischemia in rats. International Journal of Molecular Sciences 13: 1670–1679.PubMedCentralPubMedCrossRefGoogle Scholar
Bertoni-Freddari, C., P. Fattoretti, T. Casoli, et al. 2006. Reactive structural dynamics of synaptic mitochondria in ischemic delayed neuronal death. The Annals of the New York Academy of Sciences 1090: 26–34.CrossRefGoogle Scholar
Chen, H., C.J. Hu, Y.Y. He, et al. 2001. Reduction and restoration of mitochondrial DNA content after focal cerebral ischemia/reperfusion. Stroke 32: 2382–2387.PubMedCrossRefGoogle Scholar
Yazıcı, P., S. Alizadehshargh, and G. Güner-Akdoğan. 2009. Apoptosis: regulatory molecules, ıts relationship with diseases and apoptosis detection methods: Review. Turkiye Klinikleri Journal of Medical Sciences 29: 1677–1686.Google Scholar