| Peer-Reviewed

Khaya grandifololia Improves Cognition and Prevents Scopolamine-Induced Impairment of Brain Functions by Activating the Cholinergic and Antioxidant Systems in Rats

Received: 23 May 2022    Accepted: 14 June 2022    Published: 27 June 2022
Views:       Downloads:
Abstract

Alzheimer’s disease (AD) is a multifactorial, progressive neurodegenerative disorder with dementia and persistent impairment of cognitive functions as the main clinical characteristics. Although signs of progress are being made in developing AD therapy, there is no effective drug capable of stopping and/or slowing down the progression of the disease. We have previously indicated in an in vitro setting of AD that Khaya grandifololia (KG) crude extract possesses antioxidant, anti-inflammatory, and neuroprotective activities. In the current work, we have evaluated the activity of KG hydroethanolic (KG-HE) extract in preventing cognitive impairment and promoting memory improvement in vivo. Results from behavioral tests indicated a significant improvement in memory performance and a delay in depression-like behavior upon treatment of rats with KG-HE extract (5, 25, and 50 mg/kg) or donepezil (1 mg/kg) as standard. Because scopolamine (1 mg/kg) impaired cognitive performance in the tail suspension test, Morris Water Maze test, and Novelty Suppressed Feeding Test, KG-HE extract (5, 25, and 50 mg/kg) or donepezil (1 mg/kg) treatment prevented scopolamine-induced performance impairment. Moreover, both KG-HE extract (5, 25, and 50 mg/kg) and donepezil (1 mg/kg) prevented the scopolamine-induced cognitive impairment by inhibiting the acetylcholinesterase activity. In addition, the brain parameters of stress oxidation (SOD, CAT, and GSH) reduced by scopolamine treatment were regulated by the administration of KG-HE extract or the standard drug donepezil. An increase in the MDA level and the phosphatase activity both in the serum and brain due to scopolamine treatment was restored by the administration of KG-HE extract or donepezil. Taken together, these results suggest that KG-HE extract improves cognition and relieves the scopolamine-induced cognitive impairment via activation of the cholinergic and anti-oxidation systems in rats.

Published in American Journal of Biomedical and Life Sciences (Volume 10, Issue 3)
DOI 10.11648/j.ajbls.20221003.15
Page(s) 84-96
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Khaya grandifololia Hydroethanolic Extract, Alzheimer Disease, Cognition, Neuroprotection, Anxiety, Depression, Cholinergic System, Stress Oxidation

References
[1] Squire, R. (1992). Memory and the hippocampus: a synthesis from findings with rats, monkeys, and humans. Psychological Review, 99, 195-231. DOI: 10.1037/0033-295x.99.2.195.
[2] Selkoe, D. J. (2001). Alzheimer's disease: Genes, Proteins, and Therapy. Physiolgical Review, 81 (2), 741-766. DOI: 10.1152/physrev.2001.81.2.741.
[3] Rabbito, A., Dulewicz, M., Kulczynska-Przybik, A., Mroczko, B. (2020). Biochemical markers in Alzheimer’s Diseases. International Journal of Molecular Sciences, 21 (6), 1089. doi: 10.3390/ijms21061989.
[4] Kuca K, Soukup O, Maresova P, Korabecny J, Nepovimova E, Klimova B, Honegr J, Ramalho TC, França TCC (2016). Current approaches against Alzheimer’s disease in clinical trials. Journal of the Brazilian Chemical Society, 27 (4), 641-649. doi.org/10.5935/0103-5053.20160048.
[5] GBD 2019 Dementia Forecasting Collaborators (2022). Estimation of the global prevalence of dementia in 2019 and forecasted prevalence in 2050: an analysis for the Global Burden of Disease Study 2019. Lancet, 7, e105-125. https://doi.org/10.1016/S2468-2667(21)00249-8
[6] Cummings, J., Blennow, K., Johnson, K., Keeley, M., Bateman, RJ., Molinuevo, JL., Touchon, J., Vellas, B., the EU/US/CTAD Task Force (2019). Anti-Tau Trials for Alzheimer’s disease: A Report from the EU/US/CTAD Task Force. Journal of Preventive Alzheimers Disease. 3 (6): 157-163. doi: 10.14283/jpad.2019.14.
[7] Alzheimer’s Disease International (2018). Démences en Africa sub-Saharienne: défis et opportunités. [Dementias in sub-Saharan Africa: challenges and opportunities]. 11 pages. https://www.alz.co.uk/africa
[8] Massi, DG., Aretoutap, MA., Kenmegne, C., Mapoure, YN. (2020). Epidémiologie hospitalière des démences à Douala, Cameroun. Revue neurologique, 176: S2-S43. https://doi.org/10.1016/j.neurol.2020.01.056
[9] Roy, A. (2018). Role of medicinal plants against Alzheimer’s disease. International Journal of Complementary and Alternative Medicine, 11 (4), 205-208. DOI: 10.15406/ijcam.2018.11.00398.
[10] Dhingra, D., Bhankher, A. (2014). Behavioral and biochemical evidences for antidepressantlike activity of palmatine in mice subjected to chronic unpredictable mild stress, Pharmacol. Rep. 66 (2014), 1–9, https://doi.org/10.1016/j.pharep.2013.06.001
[11] John, OO., Amarachi, IS., Chinazom, AP., Adaeze, E., Kale, MB., Umare, MD., Upaganlawar, AB. (2021). Phytotherapy: A promising approach for the treatment of Alzheimer’s disease. Pharmacological Research - Modern Chinese Medicine, 2021, 2 (2022): 100030. https://doi.org/10.1016/j.prmcm.2021.100030
[12] Panzella, L., Eidenberger, T., Napolitano, A. (2018). Anti-amyloid aggregation activity of black sesame pigment: toward a novel Alzheimer’s disease preventive agent. Molecules, 23, 676. doi: 10.3390/molecules23030676.
[13] Sereia A. L., de Oliveira, M. T., Baranoski, A., Marques, L. L. M., Ribeiro, F. M., Isolani, R. G., de Medeiros, D. C., Chierrito D., Lazarin-Bidoia, D., Zielinski, A. A. F., Novello, C. R., Nakamura, C. V., Mantovani, M. S., de Mello, J. C. P. (2019). In vitro evaluation of the protective effects of plant extracts against amyloid-beta peptide-induced toxicity in human neuroblastoma SH-SY5Y cells. PLoS ONE 14 (2): e0212089. doi: 10.1371/journal.pone.0212089.
[14] Sobhani, R., Pal, A. K., Bhattacharjee, A., Mitra, S., Aguan, K. (2017). Screening indigenous medicinal plants of northeast India for their anti-Alzheimer’s properties. Pharmacog. J., 9 (1): 46-54. DOI: 10.5530/pj.2017.1.9.
[15] Witter, S., Witter, R., Vilu, R., Samoson, A. (2018). Medical Plants and Nutraceuticals for Amyloid-β Fibrillation Inhibition. Journal of Alzheimer’s Disease. Reports, 2: 239-252. DOI: 10.3233/ADR-180066.
[16] Iskandar, S., Gnansounou, MS., Robin, M., Lorquin, J., Di Giorgio, C., Piccerelle, P. (2018). Antioxidant, anti-inflammatory and neuroprotective activities of a plant extract derived from traditional Chinese medicine: SuHeXiang Wan (AT000). Chemistry of Advanced Materials, 3 (2), 36-59.
[17] Seong, SH., Ali, MY., Kim, H-R., Jung, HA., Choi, JS. (2017). BACE1 inhibitory activity and molecular docking analysis of meroterpenoids from Sargassum serratifolium. Biorganic and Medicinal Chemistry, 25 (12): 3964-3970. DOI: 10.1016/j.bmc.2017.05.033.
[18] Elufioye, T., Oladele, A., Olutayo, C., Agbedahunsi, J., Adesanya, S. (2012). Ethnomedicinal study and screening of plants used for memory enhancement and anti-aging in Sagamu, Nigeria. European Journal of Medicinal Plants, 2, 262-275. DOI: 10.9734/EJMP/2012/1372.
[19] Mukaila, YO., Ajao, AA-N., Moteetee, AN. (2021). Khaya grandifoliola C. DC. (Meliaceae: Sapindales): Ethnobotany, phytochemistry, pharmacological properties, and toxicology. Journal of Ethnopharmacology, 278, 114253.
[20] Mediesse, FK., Boudjeko, T., Hasitha, A., Gangadhar, M., Mbacham, WF., Yogeeswari, P. (2018). Inhibition of lipopolysaccharide (LPS)-induced neuroinflammatory response by polysaccharide fractions of Khaya grandifoliola (C.D.C.) stem bark, Cryptolepis sanguinolenta (Lindl.) Schltr and Cymbopogon citratus Stapf leaves in raw 264.7 macrophages and U87 glioblastoma cells. BMC Complementary and Alternative Medicine, 18, 86. doi: 10.1186/s12906-018-2156-2.
[21] Njayou, FN., Amougou, AM., Tsayem, FR., Manjia, NJ., Rudraiah, S., Bradley, B., Manautou, JE., Moundipa, PF. (2015). Antioxidant fractions of Khaya grandifoliola C.D.C. and Entada Africana Guill. et Perr. induce nuclear translocation of Nrf2 in HC-04 cells. Cell Stress Chaper., 20: 991-1000. doi: 10.1007/s12192-015-0628-6.
[22] Essama, MDS., Mezui, C., Nkwengoua, ZE., Enow-Orock, EG., Tan, PV., Nyasse, B. (2016). Cytoprotective and Antioxidant Properties of the Stem Bark Aqueous extract of Khaya grandifoliola (Meliaceae) in Rats. Journal of pharmaceutical research international, 9 (2), 1-11. DOI: 10.9734/BJPR/2016/20067.
[23] Kouam, AF., Yuan, F., Njayou, FN., He, H., Tsayem, RF., Oladejo, BO., Song, F., Moundipa. PF., Gao, GF. (2017). Induction of Mkp-1 and nuclear translocation of Nrf2 by limonoids from Khaya grandifoliola C.D.C protect L-02 hepatocytes against acetaminophen-induced hepatotoxicity. Frontier in Pharmacology, 8, 653. doi: 10.3389/fphar.2017.00653.
[24] Ella, F. A., Shantaram, M., Fewou, S. N., Njayou, F. N., Deolankar, S. C., Modi, P. K., Moundipa, P. F. (2020). Prevention of β-amyloid-induced toxicity in a differentiated neuronal (IMR32) cell line by Khaya grandifololia (Welw) C. DC. International Journal of Phytomedicine, 12 (4): 107-118. DOI: 10.5138/09750185.2443.
[25] Steru, L., Chermat, R., Thierry, B., Simon, P. (1985). The tail suspension test: a new method for screening antidepressants in mice. Psychopharmacology, 85: 367-370. doi: 10.1007/BF00428203.
[26] Morris, R. (1984). Developments of a water-maze procedure for studying spatial learning in the rat. Journal Neuroscience Methods, 11, 47-60. doi: 10.1016/0165-0270(84)90007-4.
[27] Alena, L., Mingming, Z., Nathalie, C., Mark, S., Ansorge, JA., Jasmine, H., Maria, B., Josko, L., Mark, D. (2003). Altered depression-related behaviors and functional changes in the dorsal raphe nucleus of serotonin transporter-deficient mice. Biological Psychiatry, 54, 960-971. doi: 10.1016/s0006-3223(03)00696-6.
[28] Gornall, A. G., Bardawill, C. J., David, M. M. (1949). Determination of serum proteins by means of the biuret reaction. Journal of Biological Chemistry, 177 (2), 751–766.
[29] Winterbourn, C. C., Hawkins, R. E., Brain, M., Carrel, R. W. (1975). The estimation of red cell superoxide dismutase activity. Journal of Laboratory and Clinical Medicine, 85 (2), 337–341. doi.org/10.5555/uri:pii:0022214375904394.
[30] Sinha, AK. (1972). Colorimetric assay of catalase. Analytical Biochemistry, 47 (2), 389–394. doi: 10.1016/0003-2697(72)90132-7.
[31] Smith, IK., Vierheller, TL., Thorne, CA. (1988). Assay of glutathione reductase in crude tissue homogenates using 5,5'-dithiobis (2-nitrobenzoic acid). Anal of Biochemistry, 175: 408-413. doi: 10.1016/0003-2697(88)90564-7.
[32] Wills, E. (1966). Mechanisms of lipid peroxide formation in animal tissues. Biochemical Journal, 99 (3), 667–676. doi: 10.1042/bj0990667.
[33] Ellman, G. L., Courtney, K. D., Andres, V., Featherstone, R. M. (1961). A new and rapid colorimetric determination of acetylcholinesterase activity. Biochemical Pharmacology, 7 (2), 88–95. doi: 10.1016/0006-2952(61)90145-9.
[34] McAvoy, T., Nairn, A. C. (2010). Serine/Threonine Protein Phosphatase Assays. Current Protocol in Molecular Biology, 18, 18. doi: 10.1002/0471142727.mb1818s92.
[35] Kang, I-J., Jeon, Y. E., Yin, X. F., Nam, J-S., You, S. G., Hong, M. S., Jang, B. G., Kim, M-J. (2011). Butanol extract of Ecklonia cava prevents production and aggregation of beta-amyloid, and reduces beta-amyloid mediated neuronal death. Food Chemistry and Toxicology, 49, 2252-2259. doi: 10.1016/j.fct.2011.06.023.
[36] Kondziella D, Alvestad S, Vaaler A, Sonnewald U (2007). Which clinical and experimental data link temporal lobe epilepsy with depression? J. Neurochem. 103 (2007) 2136–2152, https://doi.org/10.1111/j.1471-4159.2007.04926.x
[37] Ngoupaye, G. T., Bum, E. N., Daniels, W. M. U. (2013). Antidepressant-like effects of the aqueous macerate of the bulb of Gladiolus dalenii Van Geel (Iridaceae) in a rat model of epilepsy-associated depression, BMC Complement. Altern. Med. 1 (2013) 1–8, https://doi.org/10.1186/1472-6882-13-272.
[38] Zhang FH, Wang ZM, Liu YT, Huang JS, Liang S, Wu HH, Xu YT (2019). Bioactivities of serotonin transporter mediate antidepressant effects of Acorus tatarinowii Schott, J. Ethnopharmacol. 241 (2019) 111967, https://doi.org/10.1016/j.jep.2019.111967.
[39] Gardier AM, David DJ, Jego G, Przybylski C, Jacquot C, Durier S, Gruwez B, Douvier E, Beauverie P, Poisson N, Hen R, Bourin R (2003). Effects of chronic paroxetine treatment on dialysate serotonin in 5-HT1B receptor rknockout mice, J. Neurochem. 86 (2003) 13–24, https://doi.org/10.1046/j.1471-4159.2003.01827.x.
[40] Lin SH, Chou ML, Chen WC, Lai S, Lu KH, Hao CW, Sheen LY (2015). A medicinal herb, Melissa officinalis L. Ameliorates depressive-like behavior of rats in the forced swimming test via regulating the serotonergic neurotransmitter. Journal of. Ethnopharmacology, 175, 266–272, https://doi.org/10.1016/j.jep.2015.09.018.
[41] Yang C, Yang J, Luo A, Hashimoto K (2019). Molecular and cellular mechanisms underlying the antidepressant effects of ketamine enantiomers and its metabolites. Translational Psychiatry, 9 (1), 280. https://doi.org/10.1038/s41398-019-0624-1
[42] Ngoupaye GT, Yassib FB, Nguepi Bahaneb DA, Pahayec DB, Ngo Bum E (2020). Antidepressant and anti-amnesic effects of the aqueous lyophilisate of the leaves of Leptadenia arborea on an animal model of cognitive deficit associated depression. Biomedicine and Pharmacotherapy, 130, 110603. doi: 10.1016/j.biopha.2020.110603.
[43] Ramrao MR, Burande MD, Jangme CM, Ladde SS (2018). Evaluation of nootropic effects of aqueous extract of Tridax procumbens Linn on cognitive functions in mice. Research Journal of Life Sciences Bioinformatics, Pharmaceutical and Chemical Sciences, 4 (6), 242-251. DOI: 10.26479/2018.0406.18.
[44] Maity D, Sandur VR (2019). An updated review on herbal drugs: nootropic activity and possible mechanisms. Asian Journal of Pharmaceutical and Clinical Research, 12 (6), 19-26. doi: 10.22159/ajpcr.2019.v12i6.33164.
[45] Bhanumathy, M., Harish, MS, Shivaprasad HN, Sushma G (2010). Nootropic activity of Celastrus paniculatus seed. Pharmaceutical Biology, 48 (3), 324-327. doi: 10.3109/13880200903127391.
[46] Gawande, D. Y., Goel R. K. (2015). Pharmacological validation of in-silico guided novel nootropic potential of Achyranthes aspera L. Journal of Ethnopharmacology, 175, 324-334. DOI: 10.1016/j.jep.2015.09.025.
[47] Yadav, M. K., Singh, S. K., Tripathi, J. S., Tripathi, Y. B. (2016). Medicinal plants with nootropic effect: A review. European Journal of Biomedical and Pharmaceutical Sciences, 3 (8): 128-132.
[48] Chaudhari, K. S., Tiwari, N. R., Tiwari, R. R., Sharma, R. S. (2017). Neurocognitive effect of nootropic drug Brahmi (Bacopa monnieri) in Alzheimer’s disease. Ann. Neurosci., 24, 111-122. doi: 10.1159/000475900.
[49] Mishra, S., Palanivelu, K. (2008). The effect of curcumin (turmeric) on Alzheimer’s diesase: An overview. Ann. Indian Acad. Neurol. 11, 13. DOI: 10.4103/0972-2327.40220.
[50] Rezayof, A., Darbandi, N., Zarrindast, M. R. (2008). Nicotinic acetylcholine receptors of the ventral tegmental area are involved in mediating morphinestate-dependent learning. Neurobiology of Learning and Memory, 90, 255–260. doi: 10.1016/j. nlm.2008.03.004.
[51] Yousefi, B., Nasehi, M., Khakpai, F., Zarrindast, M. R. (2012). Possible interaction of cholinergic and GABAergic systems between MS and CA1 upon memory acquisition in rats. Behavioral Brain Research, 235, 231–243. doi: 10.1016/j.bbr.2012.08.006.
[52] Kowalczyk J, Kurach Ł, Boguszewska-Czubara A, Skalicka-Woz´niak K, Kruk-Słomka M, Kurzepa J, Wydrzynska-Kuz´ma M, Biała G, Skiba A and Budzyn´ ska B (2020) Bergapten Improves Scopolamine-Induced Memory Impairment in Mice via Cholinergic and Antioxidative Mechanisms. Frontier in Neurosciences, 14, 730. doi: 10.3389/fnins.2020.00730.
[53] Chonpathompikunlert, P., Wattanathorn, J., Muchimapura, S. (2010). Piperine, the main alkaloid of Thai black pepper, protects against neurodegeneration and cognitive impairment in animal model of cognitive deficit like condition of Alzheimer’s disease. Food Chemical Toxicology, 48, 798-802. doi: 10.1016/j.fct.2009.12.009.
[54] Mali, K., Sutar, GV., Dias, RJ., Devade, OA. (2021). Evaluation of Nootropic Activity of Limonia acidissima Against Scopolamine-induced Amnesia in rats. Turkish Journal of Pharmaceutical Sciences, 18 (1), 3-9. doi: 10.4274/tjps.galenos.2019.30316.
[55] Svoboda, J., Popelikova, A., Stuchlik, J. (2017). Drugs interfering with muscarinic acetylcholine receptors and their effects on place navigation. Frontier in Psychiatry, 8, 215. doi: 10.3389/fpsyt.2017.00215.
[56] Rosas-Ballina, M., Tracey, K. J. (2009). Cholinergic control of inflammation. Journal of Internal Medicine. 265 (6), 663-679. doi: 10.1111/j.1365-2796.2009.02098.x.
[57] Uttara, B., Singh, A., Zamboni, P., Mahajan, R., (2009). Oxidative Stress and Neurodegenerative Diseases: A Review of Upstream and Downstream Antioxidant Therapeutic Options. Current Neuropharmacology, 7, 65–74. doi: 10.2174/157015909787602823.
[58] Sadiq, A, Mahmood, F., Ullah, F., Ayaz, M., Ahmad, S., Haq, FU., Khan, G., Jan, MS. (2015). Synthesis, anticholinesterase and antioxidant potentials of ketoesters derivatives of succinimides: a possible role in the management of Alzheimer’s. Chem. Cent. J., 9, 31. doi: 10.1186/s13065-015-0107-2.
[59] Kamat, PK., Kalani, A., Rai, S., Swarnkar, S., Tota, S., Nath, C., Tyagi, N. (2016). Mechanism of oxidative stress and synapse dysfunction in the pathogenesis of Alzheimer’s disease: understanding the therapeutics strategies. Molecular Neurobiology, 53, 648-661. doi: 10.1007/s12035-014-9053-6.
[60] Haider, S., Tabassum, S., Perveen, T. (2016). Scopolamine-induced greater alterations in neurochemical profile and increased oxidative stress demonstrated a better model of dementia: A comparative study. Brain Research Bulletin, 127, 234-247. doi: 10.1016/j.brainresbull.2016.10.002.
[61] Kim, J., Keum, Y-S. (2016). Nrf2, a key regulator of antioxidant with two faces towards cancer. Oxidative Medicine and Cellular Longevity, 2746457. doi: 10.1155/2016/2746457.
[62] Kellett, K. A. B., Williams, J., Vardy, ERLC., Smith, AD., Hooper, NM. (2011). Plasma alkaline phosphatase is elevated in Alzheimer’s disease and inversely correlates with cognitive function. International Journal of Molecular Epidemiological Genetic, 2 (2), 114-121.
[63] Shi, XM., Zhang, H., Zhou, ZJ., Ruan, YY., Pang, J., Zhang, L., et al. (2018). Effects of safflower yellow on beta-amyloid deposition and activation of astrocytes in the brain of APP/PS1 transgenic mice. Biomedicine and Pharmacotherapy, 98, 553–565. https://doi.org/10.1016/j.biopha.2017.12.099
[64] Hafez, HS., Ghareeb, DA., Saleh, SR., Abady, MM., El Demellawy, MA., Hussien, H., et al. (2017) Neuroprotective effect of ipriflavone against scopolamine-induced memory impairment in rats. Psychopharmacology, 234, 3037–3053. doi: 10.1007/s00213-017-4690-x.
[65] Chen, C., Li, XH., Zhang, S., Tu, Y., Wang, YM., Sun, HT. (2014). 7, 8-dihydroxyflavone ameliorates scopolamine-induced Alzheimer-like pathologic dysfunction. Rejuvenation Research, 17, 249–254. doi: 10.1089/rej.2013.1519.
[66] Youdim, KA., Shukitt-Hale, B., Joseph, JA. (2004). Flavonoids and the brain: interactions at the blood-brain barrier and their physiological effects on the central nervous system. Free Radical Biological Medicine. 37 (1 1), 1683-93. doi: 10.1016/j.freeradbiomed.2004.08.002.
[67] Schroeter, H., Spencer, J., Rice-Evans, C., Williams, R. (2001). Flavonoids protect neurons from oxidized low-density-lipoprotein-induced apoptosis involving c-Jun N-terminal kinase (JNK), c-Jun and caspase-3. Biochemical Journal, 2001; 358: 547-57. doi: 10.1042/0264-6021:3580547.
[68] Papandreou, MA., Dimakopoulou, A., Linardaki, ZI., Cordopatis, P., Klimis-Zacas, D., Margarity, M., et al. (2009). Effect of a polyphenol-rich wild blueberry extract on cognitive performance of mice, brain antioxidant markers and acetylcholinesterase activity. Behavioral Brain Research, 198 (2), 352-8. doi: 10.1016/j.bbr.2008.11.013.
Cite This Article
  • APA Style

    Fils Armand Ella, Simon Ngamli Fewou, Mario Robillard Didier Koloko, Pascal Owona, Frederic Nico Njayou, et al. (2022). Khaya grandifololia Improves Cognition and Prevents Scopolamine-Induced Impairment of Brain Functions by Activating the Cholinergic and Antioxidant Systems in Rats. American Journal of Biomedical and Life Sciences, 10(3), 84-96. https://doi.org/10.11648/j.ajbls.20221003.15

    Copy | Download

    ACS Style

    Fils Armand Ella; Simon Ngamli Fewou; Mario Robillard Didier Koloko; Pascal Owona; Frederic Nico Njayou, et al. Khaya grandifololia Improves Cognition and Prevents Scopolamine-Induced Impairment of Brain Functions by Activating the Cholinergic and Antioxidant Systems in Rats. Am. J. Biomed. Life Sci. 2022, 10(3), 84-96. doi: 10.11648/j.ajbls.20221003.15

    Copy | Download

    AMA Style

    Fils Armand Ella, Simon Ngamli Fewou, Mario Robillard Didier Koloko, Pascal Owona, Frederic Nico Njayou, et al. Khaya grandifololia Improves Cognition and Prevents Scopolamine-Induced Impairment of Brain Functions by Activating the Cholinergic and Antioxidant Systems in Rats. Am J Biomed Life Sci. 2022;10(3):84-96. doi: 10.11648/j.ajbls.20221003.15

    Copy | Download

  • @article{10.11648/j.ajbls.20221003.15,
      author = {Fils Armand Ella and Simon Ngamli Fewou and Mario Robillard Didier Koloko and Pascal Owona and Frederic Nico Njayou and Paul Fewou Moundipa},
      title = {Khaya grandifololia Improves Cognition and Prevents Scopolamine-Induced Impairment of Brain Functions by Activating the Cholinergic and Antioxidant Systems in Rats},
      journal = {American Journal of Biomedical and Life Sciences},
      volume = {10},
      number = {3},
      pages = {84-96},
      doi = {10.11648/j.ajbls.20221003.15},
      url = {https://doi.org/10.11648/j.ajbls.20221003.15},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajbls.20221003.15},
      abstract = {Alzheimer’s disease (AD) is a multifactorial, progressive neurodegenerative disorder with dementia and persistent impairment of cognitive functions as the main clinical characteristics. Although signs of progress are being made in developing AD therapy, there is no effective drug capable of stopping and/or slowing down the progression of the disease. We have previously indicated in an in vitro setting of AD that Khaya grandifololia (KG) crude extract possesses antioxidant, anti-inflammatory, and neuroprotective activities. In the current work, we have evaluated the activity of KG hydroethanolic (KG-HE) extract in preventing cognitive impairment and promoting memory improvement in vivo. Results from behavioral tests indicated a significant improvement in memory performance and a delay in depression-like behavior upon treatment of rats with KG-HE extract (5, 25, and 50 mg/kg) or donepezil (1 mg/kg) as standard. Because scopolamine (1 mg/kg) impaired cognitive performance in the tail suspension test, Morris Water Maze test, and Novelty Suppressed Feeding Test, KG-HE extract (5, 25, and 50 mg/kg) or donepezil (1 mg/kg) treatment prevented scopolamine-induced performance impairment. Moreover, both KG-HE extract (5, 25, and 50 mg/kg) and donepezil (1 mg/kg) prevented the scopolamine-induced cognitive impairment by inhibiting the acetylcholinesterase activity. In addition, the brain parameters of stress oxidation (SOD, CAT, and GSH) reduced by scopolamine treatment were regulated by the administration of KG-HE extract or the standard drug donepezil. An increase in the MDA level and the phosphatase activity both in the serum and brain due to scopolamine treatment was restored by the administration of KG-HE extract or donepezil. Taken together, these results suggest that KG-HE extract improves cognition and relieves the scopolamine-induced cognitive impairment via activation of the cholinergic and anti-oxidation systems in rats.},
     year = {2022}
    }
    

    Copy | Download

  • TY  - JOUR
    T1  - Khaya grandifololia Improves Cognition and Prevents Scopolamine-Induced Impairment of Brain Functions by Activating the Cholinergic and Antioxidant Systems in Rats
    AU  - Fils Armand Ella
    AU  - Simon Ngamli Fewou
    AU  - Mario Robillard Didier Koloko
    AU  - Pascal Owona
    AU  - Frederic Nico Njayou
    AU  - Paul Fewou Moundipa
    Y1  - 2022/06/27
    PY  - 2022
    N1  - https://doi.org/10.11648/j.ajbls.20221003.15
    DO  - 10.11648/j.ajbls.20221003.15
    T2  - American Journal of Biomedical and Life Sciences
    JF  - American Journal of Biomedical and Life Sciences
    JO  - American Journal of Biomedical and Life Sciences
    SP  - 84
    EP  - 96
    PB  - Science Publishing Group
    SN  - 2330-880X
    UR  - https://doi.org/10.11648/j.ajbls.20221003.15
    AB  - Alzheimer’s disease (AD) is a multifactorial, progressive neurodegenerative disorder with dementia and persistent impairment of cognitive functions as the main clinical characteristics. Although signs of progress are being made in developing AD therapy, there is no effective drug capable of stopping and/or slowing down the progression of the disease. We have previously indicated in an in vitro setting of AD that Khaya grandifololia (KG) crude extract possesses antioxidant, anti-inflammatory, and neuroprotective activities. In the current work, we have evaluated the activity of KG hydroethanolic (KG-HE) extract in preventing cognitive impairment and promoting memory improvement in vivo. Results from behavioral tests indicated a significant improvement in memory performance and a delay in depression-like behavior upon treatment of rats with KG-HE extract (5, 25, and 50 mg/kg) or donepezil (1 mg/kg) as standard. Because scopolamine (1 mg/kg) impaired cognitive performance in the tail suspension test, Morris Water Maze test, and Novelty Suppressed Feeding Test, KG-HE extract (5, 25, and 50 mg/kg) or donepezil (1 mg/kg) treatment prevented scopolamine-induced performance impairment. Moreover, both KG-HE extract (5, 25, and 50 mg/kg) and donepezil (1 mg/kg) prevented the scopolamine-induced cognitive impairment by inhibiting the acetylcholinesterase activity. In addition, the brain parameters of stress oxidation (SOD, CAT, and GSH) reduced by scopolamine treatment were regulated by the administration of KG-HE extract or the standard drug donepezil. An increase in the MDA level and the phosphatase activity both in the serum and brain due to scopolamine treatment was restored by the administration of KG-HE extract or donepezil. Taken together, these results suggest that KG-HE extract improves cognition and relieves the scopolamine-induced cognitive impairment via activation of the cholinergic and anti-oxidation systems in rats.
    VL  - 10
    IS  - 3
    ER  - 

    Copy | Download

Author Information
  • Laboratory of Pharmacology and Toxicology, Department of Biochemistry, Faculty of Science, University of Yaoundé 1, Yaoundé, Cameroon

  • Faculty of Health Science, Université des Montagnes, Bangangté, Cameroon

  • Laboratory of Pharmacology and Toxicology, Department of Biochemistry, Faculty of Science, University of Yaoundé 1, Yaoundé, Cameroon

  • Laboratory of Animal Physiology, Department of Animal Biology and Physiology, Faculty of Science, University of Yaoundé 1, Yaoundé, Cameroon

  • Laboratory of Pharmacology and Toxicology, Department of Biochemistry, Faculty of Science, University of Yaoundé 1, Yaoundé, Cameroon

  • Laboratory of Pharmacology and Toxicology, Department of Biochemistry, Faculty of Science, University of Yaoundé 1, Yaoundé, Cameroon

  • Sections