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IN VITRO STUDIES ON THE PROTECTIVE EFFECT OF TANNIC ACID OF U87 CELLS INDUCED BY BETA-AMYLOID

Year 2021, Volume: 5 Issue: 3, 213 - 217, 20.09.2021
https://doi.org/10.30621/jbachs.990503

Abstract

This study shows that tannic acid is an Alzheimer's disease (AD) model cell line on amyloid-beta (Aβ)-induced U87 (human astrocytoma cell line) in β-amyloid (Aβ)-induced in vitro Alzheimer's Disease (AD) model. We aimed to investigate the effects of antioxidants.In the study; Three groups were formed as the control group, the Aβ group, and the Aβ + tannic acid group obtained by adding tannic acid to the Aβ group. Firstly, the cytotoxic potential of TA in U87 cells was investigated by the colorimetric MTT (3-4,5-dimethyl-thiazolyl-2,5 diphenyltetrazolium bromide) test. To determine the antioxidant status in the cell line treated with Thymoquinone, to examine the effects of superoxide dismutase (SOD), catalase (CAT) activities, total oxidant status (TOS), and total antioxidant status (TAS) were measured by the ELISA method. When compared to the control group, the SOD, CAT, and TOS levels were significantly decreased in the U87 cell line exposed to Aβ; TAS levels were found to increase significantly. However, the application of tannic acid to the Aβ-U87 cell line significantly increased SOD, CAT, and TAS levels; It was found that it decreased the TOS level. In in vitro experiments, we determined that tannic acid has a protective effect by increasing antioxidant parameters in the amyloid beta-induced cell line.

References

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  • 25. Oh PS. Lim KT. Blocking of intracellular ROS production by phytoglycoprotein (30 kDa) causes anti-proliferation in bisphenol A-stimulated Chang liver cells. J Appl Toxicol, 2008; 28: 749-58.
  • 26. Park MY, Jeong YJ, Kang GC, Kim MH, Kim SH et al., Nitric oxide-induced apoptosis of human dental pulp cells is mediated by the mitochondria-dependent pathway. Korean J Physiol Pharmacol 2014; 18: 25-32.
Year 2021, Volume: 5 Issue: 3, 213 - 217, 20.09.2021
https://doi.org/10.30621/jbachs.990503

Abstract

References

  • 1. Lista S, Hampel H. Synaptic degeneration and neurogranin in the pathophysiology of Alzheimer's disease. Expert Rev Neurother. 2017 ;17(1):47-57.
  • 2. Yiannopoulou KG. Papageorgiou SG. Current and Future Treatments in Alzheimer Disease: An Update. Journal of Central Nervous System Disease,2020; 12: 1–12.
  • 3. Murata S, Ono R, Sugimoto T, Toba K, Sakurai T. Functional Decline and Body Composition Change in Older Adults With Alzheimer Disease: A Retrospective Cohort Study at a Japanese Memory Clinic. Alzheimer Dis Assoc Disord. 2021;01;35(1):36-43.
  • 4. Kant RVD, Goldstein LSB. Ossenkoppele R. Amyloid-β-independent regulators of tau pathology in Alzheimer disease. Nature Reviews Neuroscience; 2020; 21:21–35.
  • 5. Hardy, J. & Selkoe, D. J. The amyloid hypothesis of Alzheimer’s disease: progress and problems on the road to therapeutics. Science 2002; 297, 353–356.
  • 6. Zheng H, Koo EH. Biology and pathophysiology of the amyloid precursor protein. Mol Neurodegener. 2011;6:27.
  • 7. Talib WH, Zarga, MH, Mahasneh AN. Antiproliferative, Antimicrobial and Apoptosis Inducing Effects of Compounds Isolated from Inula viscosa. Molecules, 2012; 17: 3291-3303
  • 8. Dinamarca MC, Cerpa W, Garrido J, Hancke JL, Inestrosa NC. Hyperforinprevents betaamyloidneurotoxicity and spatial memory impairments by disaggregation of Alzheimer's amyloidbeta-deposits. MolPsychiatry, 2006, 11:1032--1048.
  • 9. A Nordberg. Mechanisms behind the neuroprotective actions of cholinesterase inhibitors in Alzheimer disease Alzheimer Dis Assoc Disord, 2006;20, S12-S18
  • 10. Dinamarca MC, Cerpa W, Garrido J, Hancke JL, Inestrosa NC. Hyperforinprevents betaamyloidneurotoxicity and spatial memory impairments by disaggregation of Alzheimer's amyloidbeta-deposits. MolPsychiatry, 2006, 11(11):1032--1048.
  • 11. Talib WH, Zarga MH, Mahasneh AN. Antiproliferative, Antimicrobial and Apoptosis Inducing Effects of Compounds Isolated from Inulaviscosa. Molecules, 2012, 17: 3291-3303
  • 12. S. Aswathy Aromal and D. Philip, “Facile one-pot synthesis of gold nanoparticles using tannic acid and its application in catalysis,” Physica E, vol. 44, no. 7-8, pp. 1692–1696, 2012.
  • 13. Braidy N, Jugder BE, Poljak A, Jayasena T, Nabavi SM, Sachdev P, Grant R. Molecular Targets of Tannic Acid in Alzheimer's Disease. Curr Alzheimer Res. 2017;14(8):861-869. 14. Gonsette RE (2008) Neurodegeneration in multiple sclerosis: the role of oxidative stress and excitotoxicity. J Neurol Sci 274:48–53
  • 15. Mattioli R, Francioso A, d’Erme, Trovato M, Mancini P, Piacentini L, Casale AM, Wessjohann L, Gazzino R, Costantino P, Mosca L (2019) Anti-inflammatory activity of a Polyphenolic extract from Arabidopsis thaliana in in vitro and in vivo models of Alzheimer’s disease. Int J Mol Sci 20:708–727Janı KP.
  • 16. Serrano-Pozo, A., M. P. Frosch, E. Masliah and B. T. Hyman. Neuropathological alterations in Alzheimer disease.2011; Cold Spring Harb Perspect Med 1(1): a006189.
  • 17. Clark IA and Vissel B: Amyloid β: One of three danger-associated molecules that are secon-dary inducers of the proinflammatory cytokines that mediate Alzheimer's disease. Br J Phar-macol. 172:3714–3727. 2015.
  • 18. Castellani, R. J., R. K. Rolston and M. A. Smith. Alzheimer disease. Dis Mon., 2010; 56(9): 484-546. 19. Arikanoglu A. Akil E. Varol S. Yucel Y. Yuksel H. et al., Relationship of cognitive performance with prolidase and oxidative stress in Alzheimer disease. Neurol Sci 2013; 34(12):2117-21. 20. Arslan ME. Türkez H. Mardinoğlu A. In vitro neuroprotective effects of farnesene sesquiterpene on alzheimer’s disease model of differentiated neuroblastoma cell line, International Journal of Neuroscience, 2020.
  • 21. Gsell W, Conrad R, Hickethier M, Sofic E, Frolich L, Wichart I, Jellinger K, Moll G, Rnsmayr G, Beckmann H et al. Decreased Catalase Activity but Unchanged Sueroxide-Dismutase Activity in Brains of Patients with Dementia of Alzheimer-Tye. J Neurochem 1995, 64(3):1216-1223
  • 22. Kumar R. Lal N. Nemaysh V. Luthra PM. Demethoxycurcumin mediated targeting of MnSOD leading to activation of apoptotic pathway and inhibition of Akt/NF-κB survival signalling in human glioma U87 MG cells. Toxicology and Applied Pharmacology; 2018; (345):75-93.
  • 23. Mohandas E, Rajmohan V, Raghunath B. Neurobiology of Alzheimer's disease. Indian journal of psychiatry,2009; 51(1), 55. 54
  • 24. Wang P, Luo Q, Qiao H, Ding H, Cao Y, Yu J, Liu R, Zhang Q, Zhu H, Qu L. The Neuroprotective Effects of Carvacrol on Ethanol-Induced Hippocampal Neurons Impairment via the Antioxidative and Antiapoptotic Pathways. Oxid Med Cell Longev, 2017; 2017: 4079425.
  • 25. Oh PS. Lim KT. Blocking of intracellular ROS production by phytoglycoprotein (30 kDa) causes anti-proliferation in bisphenol A-stimulated Chang liver cells. J Appl Toxicol, 2008; 28: 749-58.
  • 26. Park MY, Jeong YJ, Kang GC, Kim MH, Kim SH et al., Nitric oxide-induced apoptosis of human dental pulp cells is mediated by the mitochondria-dependent pathway. Korean J Physiol Pharmacol 2014; 18: 25-32.
There are 23 citations in total.

Details

Primary Language English
Subjects Health Care Administration
Journal Section Research Article
Authors

Gülüzar Özbolat 0000-0002-3487-1088

Ares Alizade 0000-0003-0334-8152

Publication Date September 20, 2021
Submission Date September 3, 2021
Published in Issue Year 2021 Volume: 5 Issue: 3

Cite

APA Özbolat, G., & Alizade, A. (2021). IN VITRO STUDIES ON THE PROTECTIVE EFFECT OF TANNIC ACID OF U87 CELLS INDUCED BY BETA-AMYLOID. Journal of Basic and Clinical Health Sciences, 5(3), 213-217. https://doi.org/10.30621/jbachs.990503
AMA Özbolat G, Alizade A. IN VITRO STUDIES ON THE PROTECTIVE EFFECT OF TANNIC ACID OF U87 CELLS INDUCED BY BETA-AMYLOID. JBACHS. September 2021;5(3):213-217. doi:10.30621/jbachs.990503
Chicago Özbolat, Gülüzar, and Ares Alizade. “IN VITRO STUDIES ON THE PROTECTIVE EFFECT OF TANNIC ACID OF U87 CELLS INDUCED BY BETA-AMYLOID”. Journal of Basic and Clinical Health Sciences 5, no. 3 (September 2021): 213-17. https://doi.org/10.30621/jbachs.990503.
EndNote Özbolat G, Alizade A (September 1, 2021) IN VITRO STUDIES ON THE PROTECTIVE EFFECT OF TANNIC ACID OF U87 CELLS INDUCED BY BETA-AMYLOID. Journal of Basic and Clinical Health Sciences 5 3 213–217.
IEEE G. Özbolat and A. Alizade, “IN VITRO STUDIES ON THE PROTECTIVE EFFECT OF TANNIC ACID OF U87 CELLS INDUCED BY BETA-AMYLOID”, JBACHS, vol. 5, no. 3, pp. 213–217, 2021, doi: 10.30621/jbachs.990503.
ISNAD Özbolat, Gülüzar - Alizade, Ares. “IN VITRO STUDIES ON THE PROTECTIVE EFFECT OF TANNIC ACID OF U87 CELLS INDUCED BY BETA-AMYLOID”. Journal of Basic and Clinical Health Sciences 5/3 (September 2021), 213-217. https://doi.org/10.30621/jbachs.990503.
JAMA Özbolat G, Alizade A. IN VITRO STUDIES ON THE PROTECTIVE EFFECT OF TANNIC ACID OF U87 CELLS INDUCED BY BETA-AMYLOID. JBACHS. 2021;5:213–217.
MLA Özbolat, Gülüzar and Ares Alizade. “IN VITRO STUDIES ON THE PROTECTIVE EFFECT OF TANNIC ACID OF U87 CELLS INDUCED BY BETA-AMYLOID”. Journal of Basic and Clinical Health Sciences, vol. 5, no. 3, 2021, pp. 213-7, doi:10.30621/jbachs.990503.
Vancouver Özbolat G, Alizade A. IN VITRO STUDIES ON THE PROTECTIVE EFFECT OF TANNIC ACID OF U87 CELLS INDUCED BY BETA-AMYLOID. JBACHS. 2021;5(3):213-7.