α-黄檀烯:一种治疗鱼藤酮诱导帕金森病的有前途的天然药物。

Ravi Kumar, Swamita Arora, Sanjar Alam, Mohammad Rashid, Shivendra Kumar
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引用次数: 0

摘要

帕金森病(PD)是一种神经退行性疾病,其特征是黑质中多巴胺能神经元的进行性丧失,导致运动功能障碍和非运动症状。目前的治疗主要提供症状缓解而不停止疾病进展。这推动了对具有神经保护特性的天然化合物的探索。在以前的研究中,α-茶树烯,一种存在于各种芳香植物精油中的单萜,已经显示出减轻神经退行性过程的希望。本研究的重点是在鱼藤素诱导的帕金森病模型中α -茶树烯的治疗潜力。鱼藤酮是一种线粒体复合物I抑制剂,在实验模型中通常用于诱导PD样症状,因为它能够模拟人类PD中观察到的神经退行性过程。我们的综述探讨了-茶树烯的神经保护作用,重点是其抗氧化、抗炎和抗凋亡的特性。实验组的啮齿动物接受鱼藤酮诱导pd样症状,然后接受α -茶树烯治疗。进行生化分析以测量脑组织中的氧化应激标志物、炎症细胞因子和凋亡信号。结果表明,给药可显著改善大鼠运动功能,减少鱼藤酮诱导的多巴胺能神经元氧化应激、炎症和凋亡。组织病理学检查显示,与对照组相比,治疗组的神经元完整性得到了显著的保存。总之,在鱼藤素诱导的帕金森模型中,-茶树烯显示出相当大的神经保护作用。这些发现提示-茶树烯可能是一种很有前景的PD天然治疗剂,值得进一步研究其作用机制和潜在的临床应用。具体来说,我们的综述表明,-茶兰烯可能通过多种机制发挥神经保护作用,如减少氧化应激,调节神经递质水平,或抑制神经炎症。这些机制突出了其缓解PD症状和减缓疾病进展的潜力,强调了在临床环境中验证这些治疗效果的深入研究的必要性。
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α-Phellandrene: A Promising Natural Remedy for Rotenone-Induced Parkinson's Disease.

Parkinson's Disease (PD) is a neurodegenerative disorder characterized by the pro-gressive loss of dopaminergic neurons in the substantia nigra, leading to motor dysfunction and non-motor symptoms. Current treatments primarily offer symptomatic relief without halt-ing disease progression. This has driven the exploration of natural compounds with neuropro-tective properties. In previous studies, α-phellandrene, a monoterpene present in essential oils of various aromatic plants, has shown promise in mitigating neurodegenerative processes. This study focuses on alpha-phellandrene's therapeutic potential in a rotenone-induced Parkinson's Disease model. Rotenone, a mitochondrial complex I inhibitor, is commonly used to induce PD-like symptoms in experimental models due to its ability to mimic the neurodegenerative processes observed in human PD. Our review explores the neuroprotective effects of alpha-phellandrene, focusing on its antioxidant, anti-inflammatory, and anti-apoptotic properties. Experimental groups of rodents received rotenone to induce PD-like symptoms, followed by alpha-phellandrene treatment. Biochemical analyses were performed to measure oxidative stress markers, inflammatory cytokines, and apoptotic signals in brain tissues. Results indi-cated that alpha-phellandrene administration significantly improved motor function and re-duced rotenone-induced oxidative stress, inflammation, and apoptosis in dopaminergic neu-rons. Histopathological examinations revealed a notable preservation of neuronal integrity in alpha-phellandrene-treated groups compared to controls. In conclusion, alpha-phellandrene demonstrates considerable neuroprotective effects in a rotenone-induced Parkinson's dmodel. These findings suggest that alpha-phellandrene could be a promising natural therapeutic agent for PD, warranting further investigation into its mechanisms of action and potential clinical applications. Specifically, our review indicates that alpha-phellandrene may exert neuropro-tective effects by various mechanisms, such as reducing oxidative stress, modulating neuro-transmitter levels, or inhibiting neuroinflammation. These mechanisms highlight its potential to alleviate PD symptoms and slow disease progression, underscoring the need for in-depth studies to validate these therapeutic effects in clinical settings.

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