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Inflammation

, Volume 38, Issue 4, pp 1624–1630 | Cite as

Effects of Tannic Acid on the Ischemic Brain Tissue of Rats

  • Halil Murat Sen
  • Adile Ozkan
  • Mustafa Guven
  • Tarık Akman
  • Adem Bozkurt Aras
  • Ibrahim Sehitoglu
  • Hasan Alacam
  • Coskun Silan
  • Murat Cosar
  • Handan Isın Ozisik Karaman
Article

Abstract

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.

KEY WORDS

antioxidants cerebrum ischemia tannic acid 

Notes

Acknowledgments

This study was supported by the Canakkale Onsekiz Mart University Experimental Research Center (COMUDAM).

Conflict of Interest

The authors declare no conflicts of interest.

Financial Support

No financial support.

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Copyright information

© Springer Science+Business Media New York 2015

Authors and Affiliations

  • Halil Murat Sen
    • 1
  • Adile Ozkan
    • 1
  • Mustafa Guven
    • 2
  • Tarık Akman
    • 2
  • Adem Bozkurt Aras
    • 2
  • Ibrahim Sehitoglu
    • 3
  • Hasan Alacam
    • 4
  • Coskun Silan
    • 5
  • Murat Cosar
    • 2
  • Handan Isın Ozisik Karaman
    • 1
  1. 1.Department of Neurology, Faculty of MedicineCanakkale Onsekiz Mart UniversityCanakkaleTurkey
  2. 2.Department of Neurosurgery, Faculty of MedicineCanakkale Onsekiz Mart UniversityCanakkaleTurkey
  3. 3.Department of Pathology, Faculty of MedicineRecep Tayyip Erdoğan UniversityRizeTurkey
  4. 4.Department of Medical Biochemistry, Faculty of MedicineHacettepe UniversityAnkaraTurkey
  5. 5.Department of Pharmacology, Faculty of MedicineCanakkale Onsekiz Mart UniversityCanakkaleTurkey

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