Parkinson's disease is a leading hypokinetic disorder characterized by selective loss of dopaminergic neurons in substantia nigra pars compacta (SNpc) region of mid-brain. Degeneration of dopaminergic neurons is considered to be due to oxidative stress, neuroinflammation, disturbed calcium homeostasis and glutamate excitotoxicity etc. Spermidine is a polyamine which counteracts age associated cell death by scavenging free radical formation, activates authophagic machinery by enhancing formation of autophagosome, and antagonizes NMDA receptor. In the current study we investigated the neuroprotective potential of spermidine against rotenone induced PD in rats. Rats were treated subcutaneously with rotenone 1.5 mg/kg daily for 28 days. Spermidine 5&10 mg/kg was administered orally 1 h prior to rotenone administration from 15 to 28. Rotenone caused significant reduction in motor functioning and elevated levels of oxidative stress markers and proinflammatory cytokines levels (IL-1β, IL6 and TNF-α). The neurochemical analysis revealed a significant decrease in serotonin, norepinephrine, dopamine and their metabolites accompanied by a significant loss of dopaminergic neurons in the SNpc following ROT injection. However, treatment with spermidine rescued DAergic neurons in SNpc and nerve terminals in the striatum following ROT insult. Spermidine treatment also attenuated oxidative stress, neuroinflammation and restored striatal neurochemistry. Results of our study suggest that spermidine has promising neuroprotective effect against degenerative changes in experimental PD, and the protective effects are mediated through its antioxidant and anti-inflammatory properties.

帕金森氏病是一种主要的运动功能减退性疾病，其特征是大脑中部黑质致密部（SNpc）区的多巴胺能神经元选择性丢失。多巴胺能神经元的退化被认为是由于氧化应激，神经炎症，钙稳态失调和谷氨酸兴奋性毒性等引起的。亚精胺是一种多胺，通过清除自由基形成来抵消与年龄相关的细胞死亡，通过增强自噬体的形成来激活自噬机制，并拮抗。 NMDA受体。在当前的研究中，我们研究了亚精胺对鱼藤酮诱导的大鼠PD的神经保护作用。大鼠每天皮下注射鱼藤酮1.5 mg / kg皮下治疗28天。鱼藤酮给药前15至28小时，口服1 h口服亚精胺5＆10 mg / kg。鱼藤酮引起运动功能的显着降低以及氧化应激标志物和促炎细胞因子水平（IL-1β，IL6和TNF-α）的升高。神经化学分析显示，ROT注射后，SNpc中的5-羟色胺，去甲肾上腺素，多巴胺及其代谢产物显着减少，同时多巴胺能神经元也明显减少。然而，用亚精胺治疗可挽救SNpc和ROT损伤后纹状体神经末梢的DA能神经元。亚精胺治疗还可以减轻氧化应激，神经炎症和恢复纹状体神经化学。我们的研究结果表明，亚精胺对实验性PD的退行性变化具有良好的神经保护作用，其保护作用是通过其抗氧化和抗炎特性来介导的。