Abstract

Background: Brain iron deposition, low hemoglobin (HGB), and increased heme oxygenase-1 (HO-1) have been implicated in Parkinson’s disease (PD). However, the association among them in PD is poorly studied.Objective: To explore the association of the level of HO-1 with brain iron deposition and low level of HGB in PD.Methods: A total of 32 patients with PD and 26 controls were recruited for this study. C57BL/6 male mice were used in generating 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced chronic PD model. The Levels of serum HO-1 and HGB of human subjects and mice were assayed by ELISA, blood routine test, respectively. Quantitative susceptibility mapping (QSM) was used to quantitatively analyze brain iron deposition in human subjects and mice. HO-1 inhibitor (Sn-protoporphyrin, SnPP) was used to suppress the function and expression of HO-1 in PD mice. Correlations between the concentration of serum HO-1 and iron deposition of the region of interests (ROIs), levels of HGB, between the three factors mentioned above, and scores of clinical scales were explored in PD patients.Results: This study revealed significant elevation of the serum HO-1 concentration, iron deposition within bilateral substantial nigra (SN), red nucleus (RN), and putamen (PUT) and decrease of HGB level in PD patients. There was a significantly positive correlation between the serum HO-1 concentration and iron deposition within SN, an inverse correlation between the serum HO-1 concentration and HGB level in PD patients. A significant increase in HO-1 expression of serum and iron deposition in SN was also observed in the PD mouse model, and the SnPP could significantly reduce iron deposition in the SN.Conclusions: The high level of HO-1 may be the common mechanism of iron deposition and low HGB in PD. Therefore, the findings presented in this study indicate that HO-1 correlates with brain iron deposition and anemia in PD.

Highlights

  • Post-mortem and in vivo studies have demonstrated that high iron content is a prominent pathophysiological feature of Parkinson’s disease (PD) (Dexter et al, 1987; Berg and Hochstrasser, 2006; Jin et al, 2011)

  • Twenty-four PD cases and 20 controls with qualified QSM images were included for analysis of brain iron deposition (Table 1)

  • The mean levels of serum heme oxygenase-1 (HO-1) were higher in the PD group than in the control group (p < 0.01)

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Summary

Introduction

Post-mortem and in vivo studies have demonstrated that high iron content is a prominent pathophysiological feature of PD (Dexter et al, 1987; Berg and Hochstrasser, 2006; Jin et al, 2011). A series of studies have demonstrated the impact of iron deposition on the pathological aggregation of alpha synuclein (Ostrerova-Golts et al, 2000; Li et al, 2010; He et al, 2015). Many theoretical hypotheses have been used to explain iron deposition in the nigrostriatal system, including an increase of iron intake, change of iron transporter, and increased permeability of the blood-brain barrier (Ward et al, 2014). No theory explains total iron deposition, the need for in-depth studies. Low hemoglobin (HGB), and increased heme oxygenase-1 (HO-1) have been implicated in Parkinson’s disease (PD). The association among them in PD is poorly studied

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