PMID: 

Biosci Biotechnol Biochem. 2019 Dec 3:1-8. Epub 2019 Dec 3. PMID: 31791192

Abstract Title: 

Effects of genistein on lipopolysaccharide-induced injury of mouse alveolar epithelial cells and its mechanism.

Abstract: 

Alveolar and bronchial epithelial cells have critical functions in acute respiratory distress syndrome progress. Genistein could protect the lungs from acute lung injury, however, whether genistein protects the alveolar epithelial cells from LPS-induced injury was less studied. Spectrophotometric method 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) and enzyme-linked immunosorbent assay (ELISA) were performed to detect cell viability and levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6. Flow cytometry and western blot assay were performed to detect cells apoptosis and protein levels. In LPS-induced model of mouse lung epithelial (MLE)-12 cells, PBEF (proinflammatory cytokine) expression, and cell apoptosis were increased and cell viability was decreased, whereas NF-κB was activated and expression levels of TNF-α, IL-1β, and IL-6 were increased. However, genistein partly reversed the effect of LPS, and it plays a protective role in lung injury by reducing expression of PBEF, inhibiting the activation of NF-κB and alleviatinginflammatory response of cells.

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PMID: 

Phytother Res. 2019 Dec 3. Epub 2019 Dec 3. PMID: 31795012

Abstract Title: 

Genistein protects against amyloid-beta-induced toxicity in SH-SY5Y cells by regulation of Akt and Tau phosphorylation.

Abstract: 

Alzheimer's disease is a neurodegenerative disorder characterized by extracellular deposition of amyloid-β (Aβ) peptide and hyperphosphorylation of Tau protein, which ultimately leads to the formation of intracellular neurofibrillary tangles and cell death. Increasing evidence indicates that genistein, a soy isoflavone, has neuroprotective effects against Aβ-induced toxicity. However, the molecularmechanisms involved in its neuroprotection are not well understood. In this study, we have established a neuronal damage model using retinoic-acid differentiated SH-SY5Y cells treated with different concentrations of Aβto investigate the effect of genistein against Aβ-induced cell death and the possible involvement of protein kinase B (PKB, also termed Akt), glycogen synthase kinase 3β (GSK-3β), and Tau as an underlying mechanism to this neuroprotection. Differentiated SH-SY5Y cells were pre-treated for 24 hr with genistein (1 and 10 nM) and exposed to Aβ(25 μM), and we found that genistein partially inhibited Aβ induced cell death, primarily apoptosis. Furthermore, the protective effect of genistein was associated with the inhibition of Aβ-induced Akt inactivation and Tau hyperphosphorylation. These findings reinforce the neuroprotective effectsof genistein against Aβ toxicity and provide evidence that its mechanism may involve regulation of Akt and Tau proteins.

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PMID: 

Diabetol Metab Syndr. 2019 ;11:111. Epub 2019 Dec 19. PMID: 31890045

Abstract Title: 

The effect of genistein on lipid levels andandexpression in postmenopausal women with hyperlipidemia.

Abstract: 

Background: This study investigates the effect of genistein (Gen) on the lipid profiles and expression of low-density lipoprotein receptor (LDLR), liver X receptorα (LXRα) and ATP-binding cassette transporter G1 (ABCG1) in the plasma macrophages of postmenopausal women with hyperlipidemia in China.Methods: This study considered 187 cases, where 160 postmenopausal women had hyperlipidemia. The subjects were divided into placebo group (PG) and experimental group (EG). EG received 60 mg/day of Gen, PG received placebo for 6 months. Body weight, height, waist circumference, body mass index and glucose levels were determined according to standard operating procedures. The triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), apolipoprotein-A1 (Apo-A1) and apolipoprotein-B (Apo-B) levels were detected in the plasma macrophages using ELISA. The protein and mRNA expression levels of LDLR, LXRα and ABCG1 were detected by western blot and real-time PCR techniques, respectively.Results: Compared to the baseline, Gen effectively lowered TG, TC and LDL-C levels, whereas HDL-C levels as well as the protein and mRNA expression levels of LDLR, LXRα and ABCG1 ( 

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PMID: 

J Agric Food Chem. 2020 Jan 1. Epub 2020 Jan 1. PMID: 31893634

Abstract Title: 

Health Benefit of the Flavonoids from Onion: Constituents and Their Pronounced Antioxidant and Anti-neuroinflammatory Capacities.

Abstract: 

Onion is the most widely cultivated vegetables around the world. In this study, the isolation, concentration, quantification and bioactivity evaluation of the phenolics in onion peels were investigated. Thirty-four phenolics, including 17 flavonoids and 17 non-flavonoids phenolics, were purified and identified. Among them, there were 2 new unusual epoxyflavanones and a new phenolic, as well as 13 unreported constituents from the genus of Allium. The total flavonoids were concentrated and finally obtained 90.25% flavonoids content extract. Fifteen main flavonoids were quantified using UPLC-PDA, and quercetin (36.94%) and quercetin 4-O-β-D-glucopyranoside (15.81%) were the richest flavonoids in content. The antioxidant and anti-neuroinflammatory capacities were evaluated and the bioactive results indicated that the flavonoids in onion exhibited pronounced activities. The study suggested that the flavonoids in onion peels could be used in functional food.

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PMID: 

Int J Environ Res Public Health. 2019 09 6 ;16(18). Epub 2019 Sep 6. PMID: 31489898

Abstract Title: 

Ambient Air Pollution and Sudden Infant Death Syndrome in Korea: A Time-Stratified Case-Crossover Study.

Abstract: 

Sudden infant death syndrome (SIDS) is an occasional cause of unexpected mortality in infancy. While various etiological factors have been hypothesized, air pollution has been consistently presented as an environmental factor. In this study, we aimed to estimate the risk of SIDS in relation to exposure to air pollution and the effects of its modifying factors. A mortality dataset with supplementary infant mortality survey data from Statistics Korea was used and combined the concentration of ambient air pollution data from AirKorea based on the date of death and residential addresses of the SIDS cases. Odds ratios (ORs) were estimated according to birthweight, gestational age, maternal age, and infant age using a time-stratified case-crossover study design. The risk of exposure to particulate matter of less than 10μm in diameter (PM), nitrogen dioxide (NO), carbon monoxide (CO), and sulfur dioxide was estimated. The number of deaths due to SIDS was 454 (253 males and 201 females). The OR per 27.8µg/mincrement of PMwas 1.14 (95% confidence interval [CI]: 1.03-1.25) and that per 215.8 ppb of CO was 1.20 (95% CI: 1.03-1.40) in all infants. In females, an increase in NOand CO levels was associated with a higher risk of SIDS in low-birthweight and preterm infants. The OR per 15.7 ppb increment in NOwas highest among preterm infants, with a value of 5.12 (95% CI: 1.27-20.63), and low-birthweight individuals, with a value of 4.11 (95% CI: 1.74-9.72), at a moving average of 0 to 3 days. In males, however, no significant association was found. In the present study, exposure to air pollution was associated with an increased risk of SIDS. This association was more evident in susceptible infants with a low-birthweight or in cases of preterm birth.

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PMID: 

Environ Sci Pollut Res Int. 2019 Nov ;26(31):32029-32039. Epub 2019 Sep 6. PMID: 31493084

Abstract Title: 

Association between ambient air pollution exposure and infants small for gestational age in Huangshi, China: a cross-sectional study.

Abstract: 

Small for gestational age (SGA) is defined as intrauterine growth retardation or small sample, referring to the 10th percentile of birth weight lower or two standard deviations less than the average weight at the same gestational age. SGA infants bring great economic and psychological burdens to families and society. The association between exposure to air pollution and SGA in underdeveloped cities with poor air quality remains unclear. Thus, this study is conducted to estimate the effects of maternal exposure to air pollutants on SGA numbers. Birth information was collected from the Huangshi Maternity and Children's Health Hospital from January 1st to December 31st in 2017. Data of pregnancy exposure were accessed using stationary monitors. These data included particulate matter less than or equal to 10μm in aerodynamic diameter (PM), particulate matter less than or equal to 2.5μm in aerodynamic diameter (PM), nitrogen dioxide (NO), and sulfur dioxide (SO). Multivariate logistic regression models were performed to estimate the association between ambient air pollution and the risk of SGA during different exposure windows. It was found that a 1μg/mincrease in air pollution concentrations during the entire pregnancy was associated with a higher risk of SGA, with an adjusted odds ratio (OR) and 95% confidence interval (CI) of 1.055 (1.035-1.076), 1.084 (1.053-1.116), 1.000 (0.953-1.049), and 1.051 (0.968-1.141) for PM, PM, NO, and SO, respectively. Thus, it is suggested that exposure to air pollution is associated with an increased risk of SGA. The effects of PMand PMwere more stable than NOand SO.

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PMID: 

Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2019 Aug 20 ;37(8):561-566. PMID: 31495106

Abstract Title: 

[The effect of PM(2.5) on oncogene expression in HBE cells].

Abstract: 

To study the effect of particulate matter 2.5 (PM(2.5)) on oncogene expression in human bronchial epithelial (HBE) cells.HBE cells were selected as the study subjects, and PM(2.5) treatment group (10μg/ml and 50 μg/ml) , negative control group and positive control group (10 μmol/L Cr(6+)) were set. CCK8 assay was used to test the IC(50) value of PM(2.5). HBE cells were treated with PM(2.5) for 24 h at 10 μg/ml and 50 μg/ml, additionally, cells were treated with blank as negative control, 10 μmol/L Cr(6+) as a positive control for 24 h. After the treatment, mRNA expression of oncogenes including c-myc, c-fos, k-ras and p53 were detected by fluorescent quantitative RT-PCR, the protein expression of oncogenes were detected with western blot.The IC(50) value of PM(2.5) in HBE cells is 70.12μg/ml. The qRT-PCR data showed that compared with the control group, the expression level of c-myc gene increased by respectively 500.1%、780.7%、305.3% after exposure to 10、50 μg/ml PM(2.5) and positive control group; c-fos gene increased respectively 34.0%、76.7%、131.3% after exposure to10、50 μg/ml PM(2.5) and positive control group; k-ras gene increased respectively 50.3%、107.0%、49.7% after exposure to 10、50 μg/ml PM(2.5) and positive control group; p53 gene decreased by 28.3%、28.7%、59.7% after exposure to 10、50 μg/ml PM(2.5) and positive control group. The western blot results showed that compared with the control group, c-myc protein increased respectively 29.7%、77.3% after exposure to 50 μg/ml PM(2.5) and positive control group; c-fos protein increased respectively 200.3%、137.0% after exposure to 50 μg/ml PM(2.5) and positive control group; k-ras protein increased respectively 106.3%、130.3%、116.7% after exposure to 10、50 μg/ml PM(2.5) and positive control group; p53 protein decreased by 43.7%、53.3%、52.1% after exposure to 10、50 μg/ml PM(2.5) and positive control group.PM(2.5) could promote the expression of oncogenes in HBE cells, the carcinogenicity of haze might be related to promotion of oncogenes expression induced by PM(2.5).

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PMID: 

Ecotoxicol Environ Saf. 2019 Dec 30 ;190:110120. Epub 2019 Dec 30. PMID: 31896475

Abstract Title: 

Hazardous effects of urban air particulate matter acute exposure on lung and extrapulmonary organs in mice.

Abstract: 

Air particulate matter (PM) can lead to extrapulmonary adverse reactions in organs such as liver and heart either by particle translocation from the lung to the systemic circulation or by the release of lung mediators. Young BALB/c mice were intranasal instilled with 1mg/BW of Urban Air Particles from Buenos Aires or Residual Oil Fly Ash. Histopathology, oxidative metabolism and inflammation on lungs and extrapulmonary organs and the systemic response were evaluated. Lung histophatological analysis supported the rise in the number of inflammatory cells in the bronchoalveolar lavage from PM-exposed animals. Also, both PM caused recruitment of inflammatory cells in the liver and heart parenchyma and IL-6 and transaminases augmentation in serum. We have shown that despite morphochemical differences, both urban air PM altered the lung and extrapulmonary organs. Therefore, exposure to urban air PM may distress body metabolism which, in turn could lead to the development and progression of multifactorial diseases.

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PMID: 

JAMA Netw Open. 2020 Jan 3 ;3(1):e1918504. Epub 2020 Jan 3. PMID: 31899531

Abstract Title: 

Association of Ambient and Household Air Pollution With Bone Mineral Content Among Adults in Peri-urban South India.

Abstract: 

Importance: Air pollution is a major threat to global health. Osteoporosis is responsible for a substantial burden of disease globally and is expected to increase in prevalence because of population aging. Few studies have investigated the association between air pollution and bone health, and their findings were inconclusive.
Objective: To quantify the association between ambient and household air pollution and bone mass in a sample of the general population in peri-urban India.
Design, Setting, and Participants: This was a population-based cross-sectional analysis of the Andhra Pradesh Children and Parents Study cohort, which recruited participants from 28 villages near Hyderabad, South India, during 2009 to 2012. Separate linear mixed models were fitted with nested random intercepts (household within villages) for each exposure-outcome pair and were sequentially adjusted for potential confounders. Data analysis was conducted between April 2019 and July 2019.
Exposures: Annual mean ambient particulate matter air pollution less than 2.5µm in aerodynamic diameter (PM2.5) and black carbon (BC) levels at the residence estimated by land-use regression and self-reported use of biomass cooking fuel.
Main Outcomes and Measures: The primary outcome was bone mineral content (BMC) measured in grams, corrected by bone area at the lumbar spine and left hip, as measured by dual-energy x-ray absorptiometry. The secondary outcome was bone mineral density measured in grams per centimeters squared.
Results: A total of 3717 participants were analyzed (mean [SD] age, 35.7 [14.0] years; 1711 [46.0%] women). The annual mean (SD) PM2.5 exposure was 32.8 (2.5)μg/m3, and the annual mean (SD) BC exposure was 2.5 (0.2) μg/m3; 57.8% of participants used biomass cooking fuels. In fully adjusted models, PM2.5 was associated with lower BMC in the spine (mean difference, -0.57 g per 3 μg/m3 increase in PM2.5; 95% CI, -1.06 to -0.07 g per 3 μg/m3 increase inPM2.5) and hip (mean difference, -0.13 g per 3 μg/m3 increase in PM2.5; 95% CI, -0.3 to 0.03 g per 3 μg/m3 increase in PM2.5). After confounder adjustment, exposure to PM2.5 was also associated with lower bone mineral density in the spine (mean difference, -0.011 g/cm2 per 3 μg/m3 increase in PM2.5; 95% CI, -0.021 to 0 g/cm2 per 3 μg/m3 increase in PM2.5) and hip (mean difference, -0.004 g/cm2 per 3 μg/m3 increase in PM2.5; 95% CI, -0.008 to 0.001 g/cm2 per 3 μg/m3 increase in PM2.5). Exposure to BC was associated with lower BMC in the spine (mean difference, -1.13 g per 1 μg/m3 increase in BC; 95% CI, -2.81 to 0.54 g per 1 μg/m3 increase in BC) and hip (mean difference, -0.35 g per 1 μg/m3 increase in BC; 95% CI, -0.96 to 0.25 g per 1 μg/m3 increase in BC), although the confidence intervals were wider. There was no association between biomass fuel use and spine BMC (mean difference, 0.12 g; 95% CI, -0.45 to 0.68 g).
Conclusions and Relevance: In a cross-sectional analysis of a population-based cohort, ambient air pollution was associated with lower BMC in a young adult population in a peri-urban area of South India.

PMID: 

Sci Total Environ. 2019 Nov 21:135146. Epub 2019 Nov 21. PMID: 31787282

Abstract Title: 

Organochlorine pesticides exposure may disturb homocysteine metabolism in pregnant women.

Abstract: 

Maternal exposure to organochlorine pesticides (OCPs) has an adverse impact on maternal and fetal health, and excessive homocysteine is related to a variety of adverse pregnancy outcomes. Biomimetic studies suggest that OCPs interfere with folate-dependent pathways, but little evidence is available from studies with human subjects. This study explored whether exposure to OCPs interferes with the metabolism of homocysteine, which is folate dependent. A total of 313 pregnant women at 12-20 weeks gestation were recruited in Shanxi province, China, from 2014 to 2015. Plasma concentrations of 20 OCPs, including dichlorodiphenyltrichloroethane and metabolites (DDTs), hexachlorobenzene (HCB), and hexachlorocyclohexanes (HCHs), were analyzed by gas chromatography-mass spectrometry. Bloodfolate concentrations were analyzed by microbiological assay, and plasma homocysteine concentrations were determined by enzyme-linked immunosorbent assay. Information on demographics, lifestyle behaviors, and folic acid supplementation was collected by in-person interview. Of the women, 99% reportedhaving taken folic acid supplements. Results of a logistic regression analysis showed that higher plasma levels of OCPs were associated with increased odds of higher plasma homocysteine after adjustment for potential confounding factors. Positive correlations were observed between plasma OCPs and plasma homocysteine concentrations: HCB (r = 0.176, p = 0.002), β-HCH (r = 0.172, p = 0.002), ρ,ρ'-DDE (r = 0.132, p = 0.020), ρ,ρ'-DDD (r = 0.161, p = 0.004), and ο,ρ'-DDT (r = 0.144, p = 0.011). Plasma concentrations of OCPs were negatively correlated with red blood cell(RBC) folate in the low-RBC-folate subgroup, but the correlations were not statistically significant. A positive correlation was observed between OCPs and homocysteine in the low-RBC-folate subgroup. These findings suggest that OCPs may disturb the folate-dependent homocysteine metabolism pathway.

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