Bee venom attenuates neurodegeneration and motor impairment and modulates the response to L-dopa or rasagiline in a mice model of Parkinson’s disease | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 16، دوره 23، شماره 12، اسفند 2020، صفحه 1628-1638 اصل مقاله (966.39 K) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2020.46469.10731 | ||
| نویسندگان | ||
| Hanaa Badawi* 1؛ Rania Abdel-Salam2؛ Omar Abdel-Salam3؛ Eman Youness4؛ Nermeen Shaffie5؛ Ezz‐El Din Eldenshary2 | ||
| 1Holding Company for Biological Products, Vaccines and Drugs (VACSERA), Cairo, Egypt | ||
| 2Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt | ||
| 3Department of Toxicology and Narcotics, National Research Centre, Cairo, Egypt | ||
| 4Department of Medical Biochemistry, National Research Centre, Cairo, Egypt | ||
| 5Department of Pathology, National Research Centre, Cairo, Egypt | ||
| چکیده | ||
| Objective(s): This study aimed to investigate the effect of bee venom, a form of alternative therapy, on rotenone-induced Parkinson’s disease (PD) in mice. Moreover, the possible modulation by bee venom of the effect of L-dopa/carbidopa or rasagiline was examined. Materials and Methods: Rotenone (1.5 mg/kg, subcutaneously; SC) was administered every other day for two weeks and at the same time mice received the vehicle (DMSO, SC), bee venom (0.065, 0.13, and 0.26 mg/kg; intradermal; ID), L-dopa/carbidopa (25 mg/kg, intraperitoneal; IP), L-dopa/carbidopa+bee venom (0.13 mg/kg, ID), rasagiline (1 mg/kg, IP) or rasagiline+bee venom (0.13 mg/kg, ID). Then, wire hanging and staircase tests were performed and mice were euthanized and brains’ striata separated. Oxidative stress biomarkers namely, malondialdehyde (MDA), nitric oxide (NO), reduced glutathione (GSH), paraoxonase-1 (PON-1), and total antioxidant capacity (TAC) were measured. Additionally, butyrylcholinesterase (BuChE), monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), and dopamine (DA) were evaluated. Brain histopathological changes and caspase-3- expression were done. Results: Bee venom significantly enhanced motor performance and inhibited rotenone-induced oxidative/nitrosative stress, observed as a reduction in both MDA and NO along with increasing GSH, PON-1, and TAC. Besides, bee venom decreased MCP-1, TNF-α, and caspase-3 expression together with an increase in BuChE activity and DA content. Conclusion: Bee venom alone or in combination with L-dopa/carbidopa or rasagiline alleviated neuronal degeneration compared with L-dopa/carbidopa or rasagiline treatment only. Bee venom via its antioxidant and cytokine reducing potentials might be of value either alone or as adjunctive therapy in the management of PD. | ||
| کلیدواژهها | ||
| Bee venom؛ Dopamine؛ Oxidative stress؛ Parkinson’s disease؛ Rotenone | ||
| مراجع | ||
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