Parkinson’s disease (PD) pathogenesis inevitably involves neuroinflammatory responses attained through contribution of both neuron and glial cells. Investigation done in both experimental models of PD and in samples of PD patients suggested the involvement of both central and peripheral inflammatory responses during PD pathogenesis. Such neuroinflammatory responses could be regulated by neuron-glia interaction which is one of the recently focused areas in the field of disease diagnosis, pathogenesis and therapeutics. Such aggravated neuroinflammatory responses during PD are very well associated with augmented levels of cyclooxygenase (COX). An increased expression of cyclooxygenase (COX) with a concomitant increase in the prostaglandin E2 (PGE2) levels has been observed during PD pathology. Ibuprofen is one of the non-steroidal anti-inflammatory drugs (NSAID) and clinically being used for PD patients. This review focuses on the neuroinflammatory responses during PD pathology as well as the effect of ibuprofen on various disease related signaling factors and mechanisms involving nitrosative stress, neurotransmission, neuronal communication and peroxisome proliferator-activated receptor-γ. Such mechanistic effect of ibuprofen has been mostly reported in experimental models of PD and clinical investigations are still required. Since oxidative neuronal death is one of the major neurodegenerative mechanisms in PD, the antioxidant capacity of ibuprofen along with its antidepressant effects have also been discussed. This review will direct the readers towards fulfilling the existing gaps in the mechanistic aspect of ibuprofen and enhance its clinical relevance in PD therapeutics and probably in other age-related neurodegenerative diseases.

帕金森病 (PD) 的发病机制不可避免地涉及通过神经元和神经胶质细胞的贡献获得的神经炎症反应。在 PD 实验模型和 PD 患者样本中进行的研究表明，在 PD 发病过程中，中枢和外周炎症反应均参与其中。这种神经炎症反应可以通过神经元-神经胶质相互作用进行调节，这是疾病诊断、发病机制和治疗领域最近关注的领域之一。PD 期间这种加重的神经炎症反应与环加氧酶 (COX) 的增加水平密切相关。在 PD 病理过程中观察到环氧合酶 (COX) 表达增加，同时前列腺素 E2 (PGE2) 水平增加。布洛芬是一种非甾体抗炎药（NSAID），临床上用于PD患者。本综述重点关注 PD 病理过程中的神经炎症反应，以及布洛芬对各种疾病相关信号因子和机制的影响，包括亚硝化应激、神经传递、神经元通讯和过氧化物酶体增殖物激活受体-γ。布洛芬的这种机械作用主要在 PD 实验模型中报道，仍需要临床研究。由于氧化性神经元死亡是 PD 的主要神经退行性机制之一，因此还讨论了布洛芬的抗氧化能力及其抗抑郁作用。