Parkinson’s disease (PD) is the second most common neurodegenerative disease, characterised by the loss of dopaminergic neurons in the substantia nigra. Mounting evidence indicates a crucial role of inflammation and concomitant oxidative stress in the disease progression. Therefore, the aim of this study was to investigate the ability of systemically administered lipopolysaccharide (LPS) to induce motor and non-motor symptoms of PD, inflammation, oxidative stress and major neuropathological hallmarks of the disease in regions postulated to be affected, including the olfactory bulb, hippocampus, midbrain and cerebellum. Twenty-one male C57BL/6 mice, approximately 20 weeks old, received a dose of 0.3 mg/kg/day of LPS systemically on 4 consecutive days and behavioural testing was conducted on days 14–18 post-treatment, followed by tissue collection. Systemically administered LPS increased latency time in the buried food seeking test (indicative of olfactory impairment), and decreased time spent in central zone of the open field (anxiety-like behaviour). However, there was no change in latency time in the rotarod test or the expression of tyrosine hydroxylase (TH) in the midbrain. Systemically administered LPS induced increased glial markers GFAP and Iba-1 and oxidative stress marker 3-nitrotyrosine (3-NT) in the olfactory bulb, hippocampus, midbrain and cerebellum, and there were region specific changes in the expression of NFκB, IL-1β, α-synuclein, TH and BDNF proteins. The model could be useful to further elucidate early non-motor aspects of PD and the possible mechanisms contributing to the non-motor deficits.

帕金森病 (PD) 是第二常见的神经退行性疾病，其特征是黑质中多巴胺能神经元的丧失。越来越多的证据表明炎症和伴随的氧化应激在疾病进展中的关键作用。因此，本研究的目的是研究全身给药的脂多糖 (LPS) 诱导 PD 的运动和非运动症状、炎症、氧化应激和假定受影响区域的疾病主要神经病理学特征的能力，包括嗅球、海马、中脑和小脑。21 只大约 20 周大的雄性 C57BL/6 小鼠连续 4 天全身接受 0.3 mg/kg/天的 LPS 剂量，并在治疗后第 14-18 天进行行为测试，然后进行组织收集。全身施用的 LPS 增加了掩埋食物寻找测试中的潜伏时间（表明嗅觉障碍），并减少了在开放区域中心区域花费的时间（焦虑样行为）。然而，旋转棒试验的潜伏期或中脑酪氨酸羟化酶 (TH) 的表达没有变化。全身给药 LPS 诱导嗅球、海马、中脑和小脑的胶质标志物 GFAP 和 Iba-1 和氧化应激标志物 3-硝基酪氨酸 (3-NT) 增加，并且 NFκB、IL-1β 的表达存在区域特异性变化、α-突触核蛋白、TH 和 BDNF 蛋白。该模型可用于进一步阐明 PD 的早期非运动方面以及导致非运动缺陷的可能机制。