Aims/hypothesis Although much is known about the pathophysiological processes contributing to diabetic retinopathy (DR), the role of protective pathways has received less attention. The transcription factor nuclear factor erythroid-2-related factor 2 (also known as NFE2L2 or NRF2) is an important regulator of oxidative stress and also has anti-inflammatory effects. The objective of this study was to explore the potential role of NRF2 as a protective mechanism in DR. Methods Retinal expression of NRF2 was investigated in human donor and mouse eyes by immunohistochemistry. The effect of NRF2 modulation on oxidative stress was studied in the human Müller cell line MIO-M1. Non-diabetic and streptozotocin-induced diabetic wild-type and Nrf2 knockout mice were evaluated for multiple DR endpoints. Results NRF2 was expressed prominently in Müller glial cells and astrocytes in both human and mouse retinas. In cultured MIO-M1 cells, NRF2 inhibition significantly decreased antioxidant gene expression and exacerbated tert-butyl hydroperoxide- and hydrogen peroxide-induced oxidative stress. NRF2 activation strongly increased NRF2 target gene expression and suppressed oxidant-induced reactive oxygen species. Diabetic mice exhibited retinal NRF2 activation, indicated by nuclear translocation. Superoxide levels were significantly increased by diabetes in Nrf2 knockout mice as compared with wild-type mice. Diabetic Nrf2 knockout mice exhibited a reduction in retinal glutathione and an increase in TNF-α protein compared with wild-type mice. Nrf2 knockout mice exhibited early onset of blood–retina barrier dysfunction and exacerbation of neuronal dysfunction in diabetes. Conclusions/interpretation These results indicate that NRF2 is an important protective mechanism regulating the progression of DR and suggest enhancement of the NRF2 pathway as a potential therapeutic strategy.

BackgroundHeavy fine particulate matter (PM2.5) air pollution occurs frequently in China. However, epidemiological research on the association between short-term exposure to PM2.5 pollution and respiratory disease morbidity is still limited. This study aimed to explore the association between PM2.5 pollution and hospital emergency room visits (ERV) for total and cause-specific respiratory diseases in urban areas in Beijing.MethodsDaily counts of respiratory ERV from Jan 1 to Dec 31, 2013, were obtained from ten general hospitals located in urban areas in Beijing. Concurrently, data on PM2.5 were collected from the Beijing Environmental Protection Bureau, including 17 ambient air quality monitoring stations. A generalized-additive model was used to explore the respiratory effects of PM2.5, after controlling for confounding variables. Subgroup analyses were also conducted by age and gender.ResultsA total of 92,464 respiratory emergency visits were recorded during the study period. The mean daily PM2.5 concentration was 102.1±73.6 μg/m3. Every 10 μg/m3 increase in PM2.5 concentration at lag0 was associated with an increase in ERV, as follows: 0.23% for total respiratory disease (95% confidence interval [CI]: 0.11%-0.34%), 0.19% for upper respiratory tract infection (URTI) (95%CI: 0.04%-0.35%), 0.34% for lower respiratory tract infection (LRTI) (95%CI: 0.14%-0.53%) and 1.46% for acute exacerbation of chronic obstructive pulmonary disease (AECOPD) (95%CI: 0.13%-2.79%). The strongest association was identified between AECOPD and PM2.5 concentration at lag0-3 (3.15%, 95%CI: 1.39%-4.91%). The estimated effects were robust after adjusting for SO2, O3, CO and NO2. Females and people 60 years of age and older demonstrated a higher risk of respiratory disease after PM2.5 exposure.ConclusionPM2.5 was significantly associated with respiratory ERV, particularly for URTI, LRTI and AECOPD in Beijing. The susceptibility to PM2.5 pollution varied by gender and age.

BackgroundResearch on the relationship between metabolic syndrome (MetS), its components and eating speed is limited in China. The present study aimed to clarify the association between MetS, its components and eating speed in a Beijing adult population.MethodsThis cross-sectional study included 7972 adults who were 18–65 years old and who received health check-ups at the Beijing Physical Examination Center in 2016. Logistic regression was conducted to explore the associations between MetS, its components and eating speed.ResultsThe prevalence of MetS in this population was 24.65% (36.02% for males and 10.18% for females). Eating speed was significantly associated with a high risk for MetS, elevated blood pressure, and central obesity for both genders. Eating speed was associated with a high risk for elevated triglycerides and with a reduction in high-density lipoprotein in males, and eating speed was associated with a high risk for elevated fasting plasma glucose in females. Compared with slow eating speed, the multivariate-adjusted odds ratios of medium eating speed and fast eating speed for MetS were 1.65 (95% confidence interval 1.32–2.07) and 2.27 (95% confidence interval 1.80–2.86) for all subjects, 1.58 (95% confidence interval 1.21–2.07) and 2.21 (95% confidence interval 1.69–2.91) for males, and 1.75 (95% confidence interval 1.15–2.68) and 2.27 (95% confidence interval 1.46–3.53) for females, respectively.ConclusionsEating speed is positively associated with MetS and its components. Future recommendations aiming to prevent MetS and its components may focus on eating speed.Electronic supplementary materialThe online version of this article (10.1186/s12889-018-5784-z) contains supplementary material, which is available to authorized users.

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