Badawi Hanaa Mm, Abdelsalam Rania M, Abdel-Salam Omar Me, Youness Eman R, Shaffie Nermeen M, Eldenshary Ezz-El Din S
Holding Company for Biological Products, Vaccines and Drugs (VACSERA), Cairo, Egypt.
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
Iran J Basic Med Sci. 2020 Dec;23(12):1628-1638. doi: 10.22038/ijbms.2020.46469.10731.
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.
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.
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.
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.
本研究旨在探讨替代疗法之一的蜂毒对小鼠鱼藤酮诱导的帕金森病（PD）的影响。此外，还研究了蜂毒对左旋多巴/卡比多巴或雷沙吉兰疗效的可能调节作用。
每隔一天皮下注射鱼藤酮（1.5mg/kg），持续两周，同时小鼠接受溶剂（二甲基亚砜，皮下注射）、蜂毒（0.065、0.13和0.26mg/kg；皮内注射）、左旋多巴/卡比多巴（25mg/kg，腹腔注射）、左旋多巴/卡比多巴+蜂毒（0.13mg/kg，皮内注射）、雷沙吉兰（1mg/kg，腹腔注射）或雷沙吉兰+蜂毒（0.13mg/kg，皮内注射）。然后，进行悬线和阶梯试验，对小鼠实施安乐死并分离脑纹状体。检测氧化应激生物标志物，即丙二醛（MDA）、一氧化氮（NO）、还原型谷胱甘肽（GSH）、对氧磷酶-1（PON-1）和总抗氧化能力（TAC）。此外，还评估了丁酰胆碱酯酶（BuChE）、单核细胞趋化蛋白-1（MCP-1）、肿瘤坏死因子-α（TNF-α）和多巴胺（DA）。进行脑组织病理学变化和半胱天冬酶-3表达检测。
蜂毒显著提高运动性能，抑制鱼藤酮诱导的氧化/亚硝化应激，表现为MDA和NO减少，同时GSH、PON-1和TAC增加。此外，蜂毒降低MCP-1、TNF-α和半胱天冬酶-3表达，同时增加BuChE活性和DA含量。
与仅用左旋多巴/卡比多巴或雷沙吉兰治疗相比，单独使用蜂毒或与左旋多巴/卡比多巴或雷沙吉兰联合使用可减轻神经元变性。蜂毒凭借其抗氧化和降低细胞因子的潜力，单独使用或作为辅助疗法在PD管理中可能具有价值。
