HAEMATOCOCCUS PLUVIALIS MODULATING EFFECT ON NEUROTRANSMITTERS, HORMONES AND OXIDATIVE DAMAGE-ASSOCIATED WITH ALZHEIMER´S DISEASE IN EXPERIMENTAL RAT´S MODEL

  • Farouk K. El-baz Plant Biochemistry Department, National Research Centre (NRC), 33 El Bohouth st. (former El Tahrirst.), Dokki, Giza, Egypt, P.O.12622
  • Hanan F. Aly Therapeutic Chemistry Department, National Research Centre (NRC), 33 El Bohouth st. (former El Tahrirst.), Dokki, Giza, Egypt, P.O.12622
  • Gamila H. Ali Water pollution Research Department, National Research Centre (NRC), 33 El Bohouth st. (former El Tahrirst.), Dokki, Giza, Egypt, P.O.12622

Abstract

Objective: This study was planned to assess the efficacy of Haematococcus pluvialis in the regression of Alzheimer’s disease (AD).

Methods: Fifty rats were divided into five groups. Positive control group orally received aluminium chloride in a dose 100 mg/kg to induce AD: AD induced rats were orally treated with H. pluvialis extract (150 mg/kg) and rivastigmine standard drug (4.6 mg/kg/day) for 30 d. Brain acetylcholine esterase (AchE), acetylcholine (Ach), dopamine (DA), adrenaline (A), noradrenaline (NA), oxidative stress biomarkers and superoxide dismutase (SOD) were determined. Further, adrenocorticotropic hormone (ACTH) and cortisol (CORT) levels were evaluated. Also, brain histopathological investigation was examined.

Results: AD induced rats recorded a significant increase in the brain AchE, concomitant with a significant decrease in Ach, DA, NA, A and SOD levels. While, a significant increase in NO and H2O2, CORT and ACTH was recorded. Moreover, brain histopathological investigation in AD rats showed the formation of amyloid plaques and necrosis of neurons. Treatment of AD induced rats with extract of H. pluvialis or standard drug resulted in an improvement in the most of the all studied biochemical parameters. Also, AD groups treated with extract or standard drug showed great improvement in the brain morphological structure with normalisation of cerebral cortex and hippocampus, though, necrosis of some cerebral neurones was detected.

Conclusion: This current study indicated that H. pluvialis extract and drug significantly ameliorates the neurotransmitters level, oxidative damage as well as pituitary function due to their anticholinesterase activity, antioxidant efficacy, beside the anti-inflammatory effect.

Keywords: Alzheimer’s disease, Haematoccus pluvialis, Anticholinesterase, neurotransmitters, Oxidative stress, Pituitary function, Neuro-inflammation, Apoptosis

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References

1. Panche A, Chandra S, Diwan Ad, Harke S. Alzheimer’s and current therapeutics: a review. Asian J Pharm Clin Res 2015;8:14-9.
2. Azam F, Amer AM, Abulifa AR, Elzwawi MM. Ginger components as new leads for the design and development of novel multi-targeted anti-Alzheimer’s drugs: a computational investigation. Drug Des Dev Ther 2014;8:2045-59.
3. Pamulaparthi A, Prathap VR, Banala M, Nanna RS. Experimental evaluation of antidepressant and antianxiety activities of aqueous leaf extracts of Senna Alata (L.) Roxb. Using in vitro animal models. Int J Curr Pharm Res 2016;8:60-3.
4. Pavandi M, Messripour M, Moshtaghi AA. Effect of Aluminium and Copper on dopamine synthesis in striatal synaptosomes of rat’s Brain. Bull Env Pharmacol Life Sci 2014;3:12-6.
5. Breydo L, Uversky VN. The role of metal ions in the aggregation of intrinsically disordered proteins in neurodegenerative diseases. Metallomics 2011;3:1163-80.
6. Sapolsky RM, Pulsinelli W. Glucocorticoids potentiate ischemic injury to neurons: therapeutic implications. Science 1985;229:1397.
7. Franceschi M, Airaghi L, Gramigna C, Truci G, Manfredi MG, Canal N, et al. ACTH and cortisol secretion in patients with Alzheimer's disease. J Neurol Neurosurg Psychiatry 1991; 54:836-37.
8. Bowen J, Soutar C, Serwata R, Lagocki S, White D, Davies S, et al. Utilization of (3S, 3. S)-astaxanthin acyl esters in pigmentation of rainbow trout (Oncorhynchusmykiss). Aquacult Nutr 2002;8:59-68.
9. Régnier P, Bastias J, Rodriguez-Ruiz V, Caballero-Casero N, Caballo C, Sicilia D, et al. Astaxanthin from Haemato-coccuspluvialis prevents oxidative stress on human endothelial cells without toxicity. Mar Drugs 2015;13:2857-74.
10. Spiler GE, Dewell A. Safety of an astaxanthin-rich Haematococcusspluvialis algal extract: a randomised clinical trial. J Med Food 2003;1:53-6.
11. Liang H, Ma A, Zhang P, Bi SL, Shi DY. Effect of ethanol extract of alga Laurencia supplementation on DNA oxidation and alkylation damage in mice. Asia Pac J Clin Nutr 2007;16:164-8.
12. Kumar V, Bal A, Gill KD. Aluminum-induced oxidative DNA damage recognition and cell cycle disruption in different regions of rat brain. Toxicology 2009;264:137-44.
13. Corey-Bloom J, Anand R, Veach J. for the ENA 713 B352 study group a randomised trial evaluating the efficacy and safety of ENA 713 (rivastigmine tartrate), a new acetylcholine esterase inhibitor, in patients with mild to moderately severe Alzheimer’s disease. Int J Geriatr Psychopharmacol 1998;1:55-65.
14. El-Baz FK, Khalil WKB, Booles HF, Aly HF, Ali GH. Dunaliellasalina suppresses oxidative stress, alterations in the expression of pro-apoptosis and inflammation-related genes induced by STZ in diabetic rats. Int J Pharm Sci Rev Res 2016;38:219-26.
15. Berkels R, Purol-Schnabel S, Roesen R. Measurement of nitric oxide by reconversion of nitrate/nitrite to nitric oxide. Methods Mol Biol 2004;279:1–8.
16. Aebi H. Catalase in vitro. Methods Enzymol 1984;105:121–6.
17. Nishikimi M, Appaji N, Yagi K. The occurrence of superoxide anion in the reaction of reduced phenazine methosulfate and molecular oxygen. Biochem Biophys Res Commun 1972;46:849–54.
18. Den Blaauwen DH, Poppe WA, Tritschler W. Acetylcholinesterase with acetylthiocholine iodide as substrate: references depending on age and sex with special reference to hormonal effects and pregnancy. J Clin Chem Clin Biochem 1983;21:381-6.
19. Oswald C, Smits SH, Hoing M, Sohn-Bosser L, Dupont L, Le Rudulier D, et al. Crystal structures of choline/acetylcholine substrate-binding protein chox from sinorhizobiummeliloti in the liganded and unliganded–closed states. J Biol Chem 2008;283:32848–59.
20. Ciarlone AF. Further modification of a fluorometric method for analyzing brain amines. Microchem J 1978;23:9-12.
21. Talbot JA, Kane JW, White A. Analytical and clinical aspects of adrenocorticotrophin determination. Ann Clin Biochem 2003;40:453.
22. Lindsay JR, Shanmugam VK, Oldfield EH. A comparison of immunometric and radioimmunoassay measurement of ACTH for the differential diagnosis of Cushing's syndrome. J Endocrinol Invest 2006;29:983.
23. Drury RA, Wallington EA. Carleton's histology technique. 4thedn. New York: Oxford University Press; 1980. p. 653-61.
24. Kumar A, Dogra S, Prakash A. Protective effect of curcumin (Curcuma longa), against aluminum toxicity: possible behavioural and biochemical alterations in rats. Behav Brain Res 2009;205:384-90.
25. Aly HF, Metwally FMM, Hanaa H, Ahmed HH. Neuroprotective effects of dehydroepiandrosterone (DHEA) in rat model of Alzheimer’s disease. Acta Biochim Pol 2011;58 :513–20.
26. Liang YQ, Tang XC. Comparative effects of huperzine A, donepezil and rivastigmine on cortical acetylcholine level and acetylcholinesterase activity in rats. Neurosci Lett 2004;361:56–9.
27. Kaur K, Kaur R, Kaur M. Recent advances in alzheimer's disease: causes and treatment. Int J Pharm Pharm Sci 2016;8:8-15.
28. Moreira PI, Carvalho C, Zhu X, Smith MA, Perry G. Mitochondrial dysfunction is a trigger of Alzheimer’s disease pathophysiology. Biochim Biophys Acta 2010;1802:2-10.
29. Hauptmann S, Scherping I, Drose S, Brandt U, Schulz KL, Jendrach M, et al. Mitochondrial dysfunction: an early event in Alzheimer pathology accumulates with age in AD transgenic mice. Neurobiol Aging 2009;30:1574–86.
30. Gibson GE, Chen HL, Xu H, Qiu L, Xu Z, Denton TT, et al. Deficits in the mitochondrial enzyme alpha-ketoglutarate dehydrogenase leads to Alzheimer’s disease like calcium dysregulation. Neurobiol Aging 2012;33:1113-24.
31. Olichon A, Landes T, Arnaune-Pelloquin L, Emorine LJ, Mils V, Guichet A. Effects of OPA1 mutations on mitochondrial morphology and apoptosis: relevance to ADOA pathogenesis. J Cell Physiol 2007;211:423–30.
32. Ahmed HH, Zaazaa AM, Abd El-Motelp BA. Zingiberofficinale and Alzheimer’s disease: evidence and mechanisms. Int J Pharm Sci Rev Res 2014;27:142-52.
33. Murray I, Duong K. Catecholamines and amyloid. Alzheimers Association 2011;7:S392–S393.
34. Sawada H, Oeda T, Yamamoto K. Catecholamines and neurodegeneration in Parkinson's disease from diagnostic marker to aggregations of α-synuclein. Diagnostics 2013;3:210-21.
35. Jomova K, Vondrakova D, Lawson M, Valko M. Metals, oxidative stress and neurodegenerative disorders. Mol Cell Biochem 2010;345:91-104.
36. Kim TS, Pae CU, Yoon SJ, Lee NJ, Kim JJ, Lee SJ. Decreased plasma antioxidants in patients with Alzheimer's disease. Int J Geriatric Psychiatry 2006;21:344-8.
37. Swaab DF, Raadsheer FC, Endert E, Hofman MA, Kamphorst W, Ravid R. Increased cortisol levels in aging and Alzheimer's disease postmortem cerebrospinal fluid. J Neuroendocrinol 1994;6:681-7.
38. Stanier RY, Kunisawa MM, Cohn-Bazire G. Purification and properties of unicellular blue, green algae (order chroococcales). Bacteriol Rev 1971;35:171-201.
39. Bihaqia SW, Sharmab M, Singhc AP, Tiwari M. Neuroprotective role of convolvulus pluricaulison aluminium induced neurotoxicity in rat brain. J Ethnopharmacol 2009;124:409–15.
40. Verma S, Szmitko PE. The vascular biology of peroxisome proliferator-activated receptors: modulation of atherosclerosis. Can J Cardiol 2006;22:12B–17B.
41. Ambati RR, Phang SM, Ravi S, Aswathanarayana RG. Astaxanthin: sources, extraction, stability, biological activities and its commercial applications a review. Mar Drugs 2014;12:128–52.
42. Chang CS, Chang CL, Lai GH. Reactive oxygen species scavenging activities in a chemiluminescence model and neuroprotection in rat pheochromocytoma cells by astaxanthin, β-carotene, and canthaxanthin. Kaohsiung J Med Sci 2013;29:412–21.
43. Guerra BA, Otton R, Impact of the carotenoid astaxanthin on phagocytic capacity, Hauptmann S, Scherping I, Drose S, et al. Mitochondrial dysfunction: an early event in Alzheimer pathology accumulates with age in AD transgenic mice. Neurobiol Aging 2009;30:1574-86.
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El-baz, F. K., H. F. Aly, and G. H. Ali. “HAEMATOCOCCUS PLUVIALIS MODULATING EFFECT ON NEUROTRANSMITTERS, HORMONES AND OXIDATIVE DAMAGE-ASSOCIATED WITH ALZHEIMER´S DISEASE IN EXPERIMENTAL RAT´S MODEL”. International Journal of Pharmacy and Pharmaceutical Sciences, Vol. 9, no. 2, Feb. 2017, pp. 198-06, doi:10.22159/ijpps.2017v9i2.15797.
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