The red blood cell distribution width (RDW) is a measure of red blood cell (RBC) size heterogeneity, which is easily calculated by dividing the SD of erythrocyte volumes for the mean corpuscular volume. Recent reporter suggested that, besides haematological diseases and anaemia, many human disorders may be closely associated with the elevated RDW. A literature review has revealed the RDW may be closely related to the development of ischaemic stroke, carotid artery atherosclerosis and cerebral embolism. Higher RDW could independently predict adverse outcomes in patients in these conditions.

Brain ischemia/reperfusion (I/R) injury is a common pathological process after ischemic stroke. Pinoresinol diglucoside (PDG) has antioxidation and antiinflammation activities. However, whether PDG ameliorates brain I/R injury is still unclear. In this study, middle cerebral artery occlusion (MCAO) model was established with male C57BL/6 mice, and the mice were treated with 5 and 10 mg/kg PDG via intravenous injection, respectively. The neurological deficit, infarct volume, and brain water content were then evaluated. HE staining and Nissl staining were used to analyze neuron injury. Besides, enzyme-linked immunosorbent assay and colorimetry assay were used to examine the level of inflammatory markers and oxidative stress markers, and Western blot was used to detect the expressions of p-p65, Nrf2, and HO-1. It was revealed that PDG could significantly alleviate the MCAO-induced neurological dysfunction of the mice and reduce the infarct volume, brain water content, and neuron injury. PDG treatment decreased the levels of TNF-α, IL-1β, IL-6, NO, ROS, and MDA, and significantly increased the activities of SOD, GSH, and GSH-Px in the brain tissue of the mice. Additionally, PDG could repress the activation of p65 and promote Nrf2 and HO-1 expressions. In conclusion, PDG exerts anti-inflammatory and antioxidation effects via regulating the NF-κB pathway and Nrf2/HO-1 pathway, thereby reducing the I/R-induced brain injury of mice.

Purpose There is growing evidence that autophagy-related gene 5 (ATG5) is involved in neural development, neuronal differentiation, and neurodegenerative diseases. The purpose of this study was to investigate the association between ATG5 gene single-nucleotide polymorphisms (SNPs) and Parkinson’s disease (PD) in the Han population. Methods A case–control study was conducted in 120 PD patients and 100 healthy volunteers. MassArray platform was used to analyze polymorphisms in three different regions of ATG5 gene (rs510432, rs573775 and rs17587319). In the included subjects, 50 PD patients and 50 healthy volunteers were selected, and the plasma ATG5 concentration was detected by enzyme-linked immunosorbent assay (ELISA). The allele and genotype frequencies of SNPs were assessed using the SHEsis program. Results We found a significant correlation between rs17587319 and PD, and the subcomponent showed a high correlation between rs17587319 with cognitive impairment and age at onset in PD patients. At the same time, the total plasma ATG5 level of PD patients and the plasma ATG5 expression level of early-onset Parkinson’s disease (EOPD) patients were significantly higher than the control group, while there was no significant difference of ATG5 expression between late-onset Parkinson’s disease (LOPD) patients and the control group. Conclusion These findings suggest that genetic variations in the ATG5 gene and low levels of the ATG5 protein are associated with susceptibility to PD and with cognitive impairment in PD patients. ATG5 could be a potential biomarker to assess the severity and prognosis of PD.

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