Neuroprotective Effect of Coffee and Tea on Haloperidol-InducedParkinson's Disease in Rat Model

Authors

  • Shaban E. A. Saad Faculty of Pharmacy, University of Tripoli Author
  • Zuhra M. Mohammed Faculty of Pharmacy, University of Tripoli Author
  • Issa E. A. Amara Faculty of Medicine, University of Zintan Author
  • Khaled Aburas .Libyan Center of Medical Research Author
  • Akram Abrahem Libyan Center of Medical Research. Author

DOI:

https://doi.org/10.54361/ljmr.16207

Keywords:

Coffee,Tea, Parkinson's disease, Haloperidol, Oxidative stress, GSH.MDA

Abstract

Background:Coffee and Tea are very popular beverages in Libyan society. They contain many bioactive substances such as polyphenols and catchiness that could have some effects for instance; antioxidant activity. The way of preparation of tea and coffee drinks are different among society. For example, in Libya tea drink is prepared by boiling the crude of fresh tea for 10 min. Therefore, the method of extraction could influence the type and quality of extracted substances. Aims: The goal of the current study was to examine the neuroprotective properties of coffee and tea beverages made by using traditional Libyan techniqueson Parkinson's disease like symptoms induced by haloperidol.Methods: Different tea and coffee beverages (treatment) were prepared and given to rats in a concentration 10%w/v for 3 consecutive weeks.Tea and coffee beverages were made as Libyans do. At day 21, rats were injected IP with 1mg/kg of haloperidol, afterward, the behavioral and motor parameters for Parkinson’s disease were tested.Results:Coffee and Tea treated groups showed significant improvement (p > 0.05)inthe behavioral activity, and in muscle coordination. Also there was a decrease in oxidation markers as treatment resulted in an elevation of glutathione reductase and decreasing in Malondialdehyde levels. In addition, the histopathological investigation showed a reduction in haloperidol induced damage in substantia nigra.Conclusion:The results showeda possible neuroprotective effect of Coffee and Tea against PD.The mechanism of protection might be due to an antioxidant activity.

References

Torquati, L., Peeters, G., Brown, W. J., & Skinner, T. L. (2018). A Daily Cup of Tea or Coffee May Keep You Moving: Association between Tea and Coffee Consumption and Physical Activity. International journal of environmental research and public health, 15(9), 1812. https://doi.org/10.3390/ijerph15091812 DOI: https://doi.org/10.3390/ijerph15091812

Zhang, Y., Yang, H., Li, S., Li, W. D., & Wang, Y. (2021). Consumption of coffee and tea and risk of developing stroke, dementia, and poststroke dementia: A cohort study in the UK Biobank. PLoS medicine, 18(11), e1003830. https://doi.org/10.1371/journal.pmed.1003830 DOI: https://doi.org/10.1371/journal.pmed.1003830

Chin, J. M., Merves, M. L., Goldberger, B. A., Sampson-Cone, A., & Cone, E. J. (2008). Caffeine content of brewed teas. Journal of analytical toxicology, 32(8), 702–704. https://doi.org/10.1093/jat/32.8.702 DOI: https://doi.org/10.1093/jat/32.8.702

Forrest, D. (1985). The world tea trade: A survey of the production, distribution and consumption of tea. Cambridge: Woodhead-Faulkner.

Awasom, I. (2011). Commodity of the quarter tea. Journal of Agriculture and Food Information,12(1), 12-22.https://doi.org/10.1080/10496505.2011.540552. DOI: https://doi.org/10.1080/10496505.2011.540552

Wang, Y., & Ho, C. T. (2009). Polyphenolic chemistry of tea and coffee: a century of progress. Journal of agricultural and food chemistry, 57(18), 8109–8114. https://doi.org/10.1021/jf804025c. DOI: https://doi.org/10.1021/jf804025c

Sekeroglu, N., Senol, F. S., Orhan, I. E., Gulpinar, A. R., Kartal, M., &Sener, B. (2012). In vitro prospective effects of various traditional herbal coffees consumed in Anatolia linked to neurodegeneration. Food research international, 45(1), 197-203.https://doi.org/10.1016/j.foodres.2011.10.008 DOI: https://doi.org/10.1016/j.foodres.2011.10.008

Kones, R. (2010). Parkinson's disease: mitochondrial molecular pathology, inflammation, statins, and therapeutic neuroprotective nutrition. Nutrition in clinical practice: official publication of the American Society for Parenteral and Enteral Nutrition, 25(4), 371–389. https://doi.org/10.1177/0884533610373932 DOI: https://doi.org/10.1177/0884533610373932

Yadav, S., Gupta, S. P., Srivastava, G., Srivastava, P. K., & Singh, M. P. (2012). Role of secondary mediators in caffeine-mediated neuroprotection in maneb- and paraquat-induced Parkinson's disease phenotype in the mouse. Neurochemical research, 37(4), 875–884. https://doi.org/10.1007/s11064-011-0682-0 DOI: https://doi.org/10.1007/s11064-011-0682-0

Meissner, W., Hill, M. P., Tison, F., Gross, C. E., &Bezard, E. (2004). Neuroprotective strategies for Parkinson's disease: conceptual limits of animal models and clinical trials. Trends in pharmacological sciences, 25(5), 249–253. https://doi.org/10.1016/j.tips.2004.03.003 DOI: https://doi.org/10.1016/j.tips.2004.03.003

Rehman, M. U., Wali, A. F., Ahmad, A., Shakeel, S., Rasool, S., Ali, R., Rashid, S. M., Madkhali, H., Ganaie, M. A., & Khan, R. (2019). Neuroprotective Strategies for Neurological Disorders by Natural Products: An update. Current neuropharmacology, 17(3),247–267. https://doi.org/10.2174/1570159X16666180911124605 DOI: https://doi.org/10.2174/1570159X16666180911124605

Saeed, A., Shakir, L., Khan, M., Ali, A., & Zaidi, A. (2017). Haloperidol induced Parkinson’s disease mice model and motor-function modulation with Pyridine-3-carboxylic acid. Biomedical Research and Therapy, 4(05),1305-1317. https://doi.org/10.15419/bmrat.v4i05.169 DOI: https://doi.org/10.15419/bmrat.v4i05.169

Hoffman, D. C., & Donovan, H. (1995). Catalepsy as a rodent model for detecting antipsychotic drugs with extrapyramidal side effect liability. Psychopharmacology, 120(2),128–133. https://doi.org/10.1007/BF02246184 DOI: https://doi.org/10.1007/BF02246184

Bogo, V., Hill, T. A., & Young, R. W. (1981). Comparison of accelerod and rotarod sensitivity in detecting ethanol- and acrylamide-induced performance decrement in rats: review of experimental considerations of rotating rod systems. Neurotoxicology, 2(4), 765–787.

Bertelli, J. A., & Mira, J. C. (1995). The grasping test: a simple behavioral method for objective quantitative assessment of peripheral nerve regeneration in the rat. Journal of neuroscience methods, 58(1-2), 151–155. https://doi.org/10.1016/0165-0270(94)00169-h DOI: https://doi.org/10.1016/0165-0270(94)00169-H

Jansone,B.,Dzirkale,Z.,Jekabsons,K.,Pilipenko,V.,Beitnere,U.,Māgure,I.,Skumbiņš,R.,Klētnieks,U.,Vanaga,I.,Muceniece,R. &Kluša,V.(2016).Spruce Needle Polyprenols Protect Against Atorvastatin-Induced Muscle Weakness and do not Influence Central Nervous System Functions in Rats. Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences.,70(1) 13-20. https://doi.org/10.1515/prolas-2016-0003 DOI: https://doi.org/10.1515/prolas-2016-0003

Barroca, N. C. B., Guarda, M. D., da Silva, N. T., Colombo, A. C., Reimer, A. E., Brandão, M. L., & de Oliveira, A. R. (2019). Influence of aversive stimulation on haloperidol-induced catalepsy in rats. Behavioural pharmacology, 30(2 and 3-Spec Issue), 229–238. https://doi.org/10.1097/FBP.0000000000000462 DOI: https://doi.org/10.1097/FBP.0000000000000462

Deacon, R. M., & Gardner, C. R. (1984). The pull-up test in rats: a simple method for evaluating muscle relaxation. Journal of pharmacological methods, 11(2), 119–124. https://doi.org/10.1016/0160-5402(84)90021-4 DOI: https://doi.org/10.1016/0160-5402(84)90021-4

Ohkawa, H., Ohishi, N., & Yagi, K. (1979). Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Analytical biochemistry, 95(2), 351–358. https://doi.org/10.1016/0003-2697(79)90738-3 DOI: https://doi.org/10.1016/0003-2697(79)90738-3

Alam, M. N., Bristi, N. J., &Rafiquzzaman, M. (2013). Review on in vivo and in vitro methods evaluation of antioxidant activity. Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society, 21(2), 143–152. https://doi.org/10.1016/j.jsps.2012.05.002 DOI: https://doi.org/10.1016/j.jsps.2012.05.002

Ellman, G. L., Courtney, K. D., Andres, V., Jr, & Featherstone, R. M. (1961). A new and rapid colorimetric determination of acetylcholinesterase activity. Biochemical pharmacology, 7, 88–95. https://doi.org/10.1016/0006-2952(61)90145-9 DOI: https://doi.org/10.1016/0006-2952(61)90145-9

Salvatore, M. F., Pruett, B. S., Dempsey, C., & Fields, V. (2012). Comprehensive profiling of dopamine regulation in substantia nigra and ventral tegmental area. Journal of visualized experiments : JoVE, (66), 4171. https://doi.org/10.3791/4171 DOI: https://doi.org/10.3791/4171-v

Kouli, A., Torsney, K. M., &Kuan, W. L. (2018). Parkinson’s disease: etiology, neuropathology, and pathogenesis. Exon Publications, 3-26. ‏ DOI: https://doi.org/10.15586/codonpublications.parkinsonsdisease.2018.ch1

Jenner P. (2003). Oxidative stress in Parkinson's disease. Annals of neurology, 53 Suppl 3, S26–S38. https://doi.org/10.1002/ana.10483 DOI: https://doi.org/10.1002/ana.10483

Waku, I., Magalhães, M. S., Alves, C. O., & de Oliveira, A. R. (2021). Haloperidol-induced catalepsy as an animal model for parkinsonism: A systematic review of experimental studies. The European journal of neuroscience, 53(11), 3743–3767. https://doi.org/10.1111/ejn.15222 DOI: https://doi.org/10.1111/ejn.15222

Greco, B., Lopez, S., van der Putten, H., Flor, P. J., &Amalric, M. (2010). Metabotropic glutamate 7 receptor subtype modulates motor symptoms in rodent models of Parkinson's disease. The Journal of pharmacology and experimental therapeutics, 332(3), 1064–1071. https://doi.org/10.1124/jpet.109.162115 DOI: https://doi.org/10.1124/jpet.109.162115

Koppula, S., Kumar, H., More, S. V., Kim, B. W., Kim, I. S., & Choi, D. K. (2012). Recent advances on the neuroprotective potential of antioxidants in experimental models of Parkinson's disease. International journal of molecular sciences, 13(8), 10608–10629. https://doi.org/10.3390/ijms130810608 DOI: https://doi.org/10.3390/ijms130810608

Chen, J. F., Xu, K., Petzer, J. P., Staal, R., Xu, Y. H., Beilstein, M., Sonsalla, P. K., Castagnoli, K., Castagnoli, N., Jr, & Schwarzschild, M. A. (2001). Neuroprotection by caffeine and A(2A) adenosine receptor inactivation in a model of Parkinson's disease. The Journal of neuroscience: the official journal of the Society for Neuroscience, 21(10), RC143.https://doi.org/10.1523/JNEUROSCI.21-10-j0001.2001 DOI: https://doi.org/10.1523/JNEUROSCI.21-10-j0001.2001

Perera, J., Tan, J. H., Jeevathayaparan, S., Chakravarthi, S., &Haleagrahara, N. (2011). Neuroprotective effects of alpha lipoic Acid on haloperidol-induced oxidative stress in the rat brain. Cell & bioscience, 1(1), 12. https://doi.org/10.1186/2045-3701-1-12 DOI: https://doi.org/10.1186/2045-3701-1-12

Jankelowitz, S.K. (2013). Treatment of neurolept-induced tardive dyskinesia. Neuropsychiatric disease and treatment, 9,1371–1380. https://doi.org/10.2147/NDT.S30767. DOI: https://doi.org/10.2147/NDT.S30767

Shivakumar, B. R., &Ravindranath, V. (1993). Oxidative stress and thiol modification induced by chronic administration of haloperidol. The Journal of pharmacology and experimental therapeutics, 265(3), 1137–1141.

Downloads

Published

31-12-2022

Issue

Section

Articles

How to Cite

1.
Saad S, Mohammed ZM, Amara IE, Aburas K, Abrahem A. Neuroprotective Effect of Coffee and Tea on Haloperidol-InducedParkinson’s Disease in Rat Model. LJMR [Internet]. 2022 Dec. 31 [cited 2024 Nov. 21];16(2):76-92. Available from: https://ljmr.ly/index.php/ljmr/article/view/39