Numerous studies have investigated the role of agmatine in the central nervous system and indicated neuroprotective properties. In addition to its potent antioxidant effects, agmatine is an endogenous neuromodulator and has wide spectrum molecular actions on different receptor subtypes (NMDA, Imidazoline 1-2, alpha-2 adrenoreceptor, 5-HT2a, 5-HT3) and cellular signaling pathways (MAPK, PKA, NO, BDNF). Although the neuroprotective effects of agmatine demonstrated in experimental Parkinson’s disease model, the effects of agmatine with the aspect of neuroplasticity and possible signaling mechanisms behind agmatine actions have not been investigated. Herein, in this study, we investigated the role of the of agmatine on rotenone-induced Parkinson’s disease model. Agmatine at the dose of 100 mg/kg i.p., was mitigated oxidative damage and alleviated motor impairments which were the results of the rotenone insult. Additionally, agmatine decrease in neuronal loss, tyrosine hydroxylase immunoreactivity and increased cREB, BDNF and ERK1/2 expression in the striatum, which are crucial neuroplasticity elements of striatal integrity. Taken together, the present study expands the knowledge of molecular mechanisms behind neuroprotective actions of agmatine in Parkinson’s disease, and as far as we have known, this is the first study to delineate agmatine treated activation of cellular pathways which are important elements in neuronal cell survival.

许多研究调查了胍丁胺在中枢神经系统中的作用，并表明了神经保护特性。除了强大的抗氧化作用外，胍丁胺还是一种内源性神经调节剂，对不同受体亚型（NMDA、咪唑啉 1-2、α-2 肾上腺素受体、5-HT2a、5-HT3）和细胞信号通路 (MAPK) 具有广谱的分子作用, PKA, NO, BDNF)。尽管在实验性帕金森病模型中证明了胍丁胺的神经保护作用，但尚未研究胍丁胺作用背后的神经可塑性和可能的​​信号传导机制方面的作用。在此，在本研究中，我们研究了胍丁胺对鱼藤酮诱导的帕金森病模型的作用。100 mg/kg ip 剂量的胍丁胺，减轻了氧化损伤并减轻了由鱼藤酮损伤引起的运动障碍。此外，胍丁胺减少了纹状体中的神经元丢失、酪氨酸羟化酶免疫反应性和增加的 cREB、BDNF 和 ERK1/2 表达，这些都是纹状体完整性的关键神经可塑性元素。总而言之，本研究扩展了对胍丁胺在帕金森病中的神经保护作用背后的分子机制的知识，据我们所知，这是第一项描述胍丁胺处理激活细胞通路的研究，这些通路是神经元细胞存活的重要因素. 这是纹状体完整性的关键神经可塑性元素。总而言之，本研究扩展了对胍丁胺在帕金森病中的神经保护作用背后的分子机制的知识，据我们所知，这是第一项描述胍丁胺处理激活细胞通路的研究，这些通路是神经元细胞存活的重要因素. 这是纹状体完整性的关键神经可塑性元素。总而言之，本研究扩展了对胍丁胺在帕金森病中的神经保护作用背后的分子机制的知识，据我们所知，这是第一项描述胍丁胺处理激活细胞通路的研究，这些通路是神经元细胞存活的重要因素.