Neuroprotective and Neurotherapeutic Effects of Bee Venom on Neurodegenerative Diseases

Abstract

Event Abstract Back to Event Neuroprotective and Neurotherapeutic Effects of Bee Venom on Neurodegenerative Diseases Miran K. Rakha1* 1 Suez Canal University, Biotechnology Research Center, Egypt Acute and chronic neurodegenerative diseases are illnesses associated with high morbidity and mortality, and few or no effective options are available for their treatment. A characteristic of many neurodegenerative diseases — which include stroke, brain trauma, spinal cord injury, amyotrophic lateral sclerosis, Huntington’s disease, Alzheimer’s disease, and Parkinson’s disease — is neuronal cell death. Given that central nervous system tissue has very limited, if any, regenerative capacity, it is of utmost importance to limit the damage caused by neuronal death. Bee venom, which is also known as apitoxin, consists of several biologically active peptides, including melittin, adolapin, mast cell degranulating peptide and phospholipase A2. Moreover, bee venom contains a variety of bioamines, such as apamin, histamine, procamine, serotonin, and norepinephrine, which facilitate nerve transmission and healing in a variety of nerve disorders. This gives bee venom the ability to travel along the neural pathways from the spine to various trigger points and injured areas to help repair nerve damage and restore mobility. This review overviews; (1) causes and mechanisms of neurodegenerative diseases which pertains to neuronal cell death, (2) evidence linking composition comprising bee venom to its substantial potential for preventing and treating of neurodegenerative diseases associated with neuronal cell death, and (3) how improving our knowledge of the mechanisms mediating neuroprotective and neurotherapeutic activities of bee venom against neuronal cell death may led to novel therapeutic strategies for the treatment of neurodegenerative diseases. Future challenges remaining will be to elucidate signaling responses activated by bee venom in neurons. In other words, bee venom inhibits neuronal cell death and activation of proapoptotic signaling in neurons. These findings emphasize the clinical importance of bee venom for treatment of neurodegenerative diseases. Further investigation is necessary to elaborate the mechanisms involved and to permit full exploitation of neuroprotective and neurotherapeutic potentials of bee venom. References Doo AR et al. (2012): Bee venom protects SH-SY5Y human neuroblastoma cells from 1-methyl-4-phenylpyridinium-induced apoptotic cell death. Brain Res, 1429: 106-115. Lee SM et al. (2012): Effects of Bee Venom on Glutamate-Induced Toxicity in Neuronal and Glial Cells. Evidence-Based Complementary and Alternative Medicine, 2012: 368196, doi:10.1155/2012/368196. Rakha MK (2011): Impact of Beehive Products on the Cardiovascular Neurophysiology Expands Novel Horizons in Apitherapy. Conference Abstract: 10th Meeting of the Société des Neurosciences, May 24-27, 2011, Marseille, France. Yang EJ et al. (2011): Melittin restores proteasome function in an animal model of ALS. J Neuroinflammation, 8: 69, doi: 10.1186/1742-2094-8-69. Yang EJ et al. (2010): Bee venom attenuates neuroinflammatory events and extends survival in amyotrophic lateral sclerosis models. J Neuroinflammation, 7: 69, doi: 10.1186/1742-2094-7-69. Keywords: Bee Venom, Neuroprotective Activity, Neurotherapeutic Potential, Neuronal Cells, Neurodegenerative Diseases. Conference: 4th Conference of the Mediterrarnean Neuroscience Society, Istanbul, Turkey, 30 Sep - 3 Oct, 2012. Presentation Type: Poster Presentation Topic: Abstracts Citation: Rakha MK (2013). Neuroprotective and Neurotherapeutic Effects of Bee Venom on Neurodegenerative Diseases. Conference Abstract: 4th Conference of the Mediterrarnean Neuroscience Society. doi: 10.3389/conf.fnhum.2013.210.00057 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 26 Jan 2013; Published Online: 11 Apr 2013. * Correspondence: Dr. Miran K Rakha, Suez Canal University, Biotechnology Research Center, Ismailia, Egypt, mirankhalil@hotmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract Supplemental Data The Authors in Frontiers Miran K Rakha Google Miran K Rakha Google Scholar Miran K Rakha PubMed Miran K Rakha Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.