de Farias Carine Coneglian, Maes Michael, Bonifacio Kamila Landucci, Matsumoto Andressa Keiko, Bortolasci Chiara Cristina, Nogueira Andre de Souza, Brinholi Francis Fregonesi, Morimoto Helena Kaminami, de Melo Lucio Baena, Moreira Estefania Gastaldello, Barbosa Decio Sabbatini
Graduation Program in Health Sciences, State University of Londrina (UEL), Parana, Brazil.
Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
CNS Neurol Disord Drug Targets. 2017;16(4):484-491. doi: 10.2174/1871527316666170223161004.
Parkinson's disease (PD) is a neurodegenerative disorder characterized by a complex interplay between peripheral and central inflammatory and oxidative stress pathways.
To investigate immune-inflammatory and oxidative stress pathways in relation to iron metabolism in peripheral blood of PD patients and healthy controls.
We recruited 56 healthy individuals and 56 PD patients in stages 1-3 of Hoehn and Yahr Scale. Plasma haptoglobin (Hp), homocysteine, interleukin 6, soluble interleukin 6 receptor, iron (Fe), ferritin, total iron binding capacity, transferrin (Tf), soluble transferrin receptor (sTfR), malondialdehyde (MDA) and paraoxonase 1 (PON1) were measured.
PD was associated with significant changes in Tf (lowered), sTfR, ferritin, Hp, interleukin 6 and MDA (all increased) levels, while there was a trend towards a negative association with PON1. Logistic regression showed that the most significant biomarkers of PD were MDA, sTfR, Hp and ferritin. Moreover, Fe levels were negatively associated with Hp and positively with PON1, total iron binding capacity and Tf, while ferritin and sTfR were positively associated with MDA levels.
Our study indicates a state of systemic inflammation and oxidative stress in PD patients coupled with alterations in Fe metabolism. Chronic inflammation and oxidative pathways in PD may in part determine changes in iron metabolism. New drug treatments for PD should target inflammatory and oxidative stress pathways and iron metabolism as well.
帕金森病(PD)是一种神经退行性疾病,其特征是外周和中枢炎症及氧化应激途径之间存在复杂的相互作用。
研究帕金森病患者和健康对照者外周血中与铁代谢相关的免疫炎症和氧化应激途径。
我们招募了56名健康个体和56名处于Hoehn和Yahr量表1 - 3期的帕金森病患者。检测血浆触珠蛋白(Hp)、同型半胱氨酸、白细胞介素6、可溶性白细胞介素6受体、铁(Fe)、铁蛋白、总铁结合力、转铁蛋白(Tf)、可溶性转铁蛋白受体(sTfR)、丙二醛(MDA)和对氧磷酶1(PON1)。
帕金森病与Tf(降低)、sTfR、铁蛋白、Hp、白细胞介素6和MDA(均升高)水平的显著变化相关,而与PON1呈负相关趋势。逻辑回归显示,帕金森病最显著的生物标志物是MDA、sTfR、Hp和铁蛋白。此外,Fe水平与Hp呈负相关,与PON1、总铁结合力和Tf呈正相关,而铁蛋白和sTfR与MDA水平呈正相关。
我们的研究表明帕金森病患者存在全身炎症和氧化应激状态,同时伴有铁代谢改变。帕金森病中的慢性炎症和氧化途径可能部分决定铁代谢的变化。帕金森病的新药治疗应同时针对炎症和氧化应激途径以及铁代谢。