中国神经再生研究(英文版) ›› 2021, Vol. 16 ›› Issue (5): 992-993.doi: 10.4103/1673-5374.297075

• 观点:退行性病与再生 • 上一篇    下一篇

羟基酪醇作为帕金森病抗炎药的证据:对作用机制的见解

  

  • 出版日期:2021-05-15 发布日期:2020-12-29

Evidences of hydroxytyrosol as an anti-inflammatory agent in Parkinson’s disease: insights into the mechanisms of action

Ruth Hornedo-Ortega, Ana María Espinosa-Oliva*   

  1. Axe Molécules d’Intérêt Biologique (MIB), Unité de Recherche Oenologie, EA4577, USC 1366 INRA, ISVV, Université de Bordeaux, Bordeaux, France (Hornedo-Ortega R)
    Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de Sevilla, and Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío/CSIC, Seville, Spain (Espinosa-Oliva AM)
  • Online:2021-05-15 Published:2020-12-29
  • Contact: Ana María Espinosa-Oliva, PhD, anaespinosa@us.es.

摘要: https://orcid.org/0000-0003-1898-8806 (Ruth Hornedo-Ortega);
https://orcid.org/0000-0002-2442-767X (Ana María Espinosa-Oliva)

Abstract: Inflammatory processes play a critical role in neurodegenerative diseases, such as Parkinson’s disease (PD). Thus, neuroinflammation is involved in the progression and development of these diseases, becoming an important pathological hallmark. Microglial cells, the “macrophages” from central nervous system, are the initiating cells of the innate immune response against different stimuli in the brain. Even though they have a major role in brain homeostasis maintenance, their uncontrolled activation results in the secretion of pro-inflammatory cytokines and production of reactive oxygen species (ROS), leading to neuronal damage and death. Microglial cells present different phenotypes, ranging from pro-inflammatory/neurotoxic to anti-inflammatory/neuroprotective phenotype, depending on the stimulants involved (Shen et al., 2018). For this reason, novel therapeutic strategies are being addressed in order to shift the microglia polarization. Among them it is worth mentioning the search for dietary bioactive compounds, which may prevent or delay the progression of neuroinflammation and, in consequence, reduce the neuronal damage caused by microglia overactivation.