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PMID: 

Int J Environ Res Public Health. 2020 Jan 1 ;17(1). Epub 2020 Jan 1. PMID: 31906378

Abstract Title: 

Bisphenol a Exposure, DNA Methylation, and Asthma in Children.

Abstract: 

Epidemiological studies have reported the relationship between bisphenol A (BPA) exposure and increased prevalence of asthma, but the mechanisms remain unclear. Here, we investigated whether BPA exposure and DNA methylation related to asthma in children. We collected urinary and blood samples from 228 children (Childhood Environment and Allergic Diseases Study cohort) aged 3 years. Thirty-three candidate genes potentially interacting with BPA exposure were selected from a toxicogenomics database. DNA methylation was measured in 22 blood samples with top-high and bottom-low exposures of BPA. Candidate genes with differential methylation levels were validated by qPCR and promoter associated CpG islands have been investigated. Correlations between the methylation percentage and BPA exposure and asthma were analyzed. According to our findings,showed differential methylation and was further investigated in 228 children. Adjusting for confounders, urinary BPA glucuronide (BPAG) level inversely correlated withpromoter methylation (β = -0.539,= 0.010). For the logistic regression analysis,methylation status was dichotomized into higher methylated and lower methylated groups with cut off continuous variable of median of promoter methylation percentage (50%) while performing the analysis.methylation was lower in children with asthma than in children without asthma (mean± SD; 69.82 ± 5.88% vs. 79.82 ± 5.56%) (= 0.001). Mediation analysis suggested thatmethylation acts as a mediation variable between BPA exposure and asthma. The mechanism of BPA exposure on childhood asthma might, therefore, be through the alteration ofmethylation. The mechanism of BPA exposure on childhood asthma might, therefore, be through the alteration ofmethylation.

PMID: 

Chemosphere. 2019 Dec 31 ;246:125775. Epub 2019 Dec 31. PMID: 31918092

Abstract Title: 

Bisphenol A and polychlorinated biphenyls enhance the cancer stem cell properties of human ovarian cancer cells by activating the WNT signaling pathway.

Abstract: 

Cancer stem cells (CSCs) are a very small subpopulation that have stem-cell qualities, such as exhibiting self-renewal, immortality, and pluripotency, and the capability to differentiate into different tumor cell subtypes. CSCs contribute to tumor onset, expansion, metastasis, resistance and recurrence. Meanwhile, organic pollutants, including nonpersistent pollutants, such as bisphenol A (BPA), and persistent pollutants, such as polychlorinated biphenyls (PCBs), are toxic chemicals that can be readily ingested via dietary exposure and other exposure routes and can accumulate through the food chain. Many organic pollutants increase the risk of ovarian cancer depending on their estrogenic effects. Nonetheless, most previous studies have focused on the toxic effects of these pollutants on the proliferation, metastasis and development of ovarian cancer cells. However, little research has investigated the adverse effect of these pollutants on ovarian cancer stem cells. The current study found that BPA, PCB126 and PCB153 greatly enhanced the formation of cancer stem-like cell spheres of OVCAR-3 cells (human ovarian cancer cells) under low-dose exposure. In parallel, the CD44CD24cell subpopulation was increased in treated cells relative to untreated cells. Elevated expression of cancer stem cell markers, including ALDH1A1, CD133, SOX2, NANOG and OCT4, was demonstrated in treated cells compared to untreated cells. In summary, these data demonstrate that the oncogenic effects of pollutants can be evaluated according to changes in caner stem cell properties.

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PMID: 

Chemosphere. 2019 Dec 31 ;246:125805. Epub 2019 Dec 31. PMID: 31918106

Abstract Title: 

Prenatal exposure to bisphenol a and its analogues (bisphenol F and S) and ultrasound parameters of fetal growth.

Abstract: 

BACKGROUND: Bisphenol A (BPA) has been shown to affect normal fetal growth, but human evidence on its analogues (BPF and BPS) is limited.OBJECT: To examine the associations between prenatal exposure to BPA and its analogues (BPF and BPS) and ultrasound parameters of fetal growth.METHODS: We measured urinary BPA, BPF, and BPS concentrations among 322 pregnant women during late pregnancy from a cohort study in Wuhan, China. Fetal biparietal diameter (BPD), head circumference (HC), femur length (FL), and abdominal circumference (AC) were measured by ultrasonography. The associations of maternal urinary BPA, BPF, and BPS concentrations with ultrasound parameters of fetal growth were estimated by multivariable adjusted models.RESULTS: We observed a gender difference in association of maternal urinary BPA concentrations and fetal HC (P for interaction = 0.003); each ln-unit increase in maternal urinary BPA concentration was associated with a mean decrease of 0.10 cm (95%CI: 0.18, -0.02) among boys and a mean increase of 0.14 cm (95%CI: 0.00, 0.28) among girls for HC. The associations were robust for urinary BPA concentrations modeled as tertiles or including urinary BPA, BPF, and BPS into mutual adjustment models. We did not observe robust associations between maternal urinary BPF and BPS concentrations and ultrasound parameters of fetal growth, though an inverse association with AC and a positive association with FL were estimated for maternal urinary BPF concentrations modeled as continuous variables.CONCLUSIONS: Prenatal exposure to BPA but not BPF and BPS was sex-specifically associated with certain fetal growth parameters.

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Alzheimer’s disease is a devastating degenerative brain condition that affects millions of people in the U.S. While pharmaceutical treatments have long lists of side effects, there is a natural food-b

Researchers find Boswellia serrata and bromelain extracts as safe and effective tools for reducing pain and inflammation in arthritis patients

Fat has long suffered a bad rap and a long-time association with poor health and disease, but research is now proving this long-held narrative false

PMID: 

Ann Ital Chir. 2019 Nov 19 ;8. Epub 2019 Nov 19. PMID: 31769414

Abstract Title: 

Comparison of the effects of thymoquinone and silymarin on the brain of rats having ischemia-reperfusion in the lower extremities.

Abstract: 

AIM: We aimed to show whether ischemia reperfusion (I/R) injury causes damage on brain or not, and whether thymoquinone and silymarin, as antioxidant and anti-inflammatory herbs, have beneficial effects on this damage or not.METHODS: Forty Wistar albino rats were carried out and were randomized to 4 groups with equal numbers (n=10): sham group, implemented of only anesthesia; control group, implemented of anesthesia and I/R injury; silymarin group, implemented of anesthesia and I/R injury and treated with a dose of 200 milligram/kg silymarin ip and thymoquinone group, implemented of anesthesia and I/R injury and treated with a dose of 20 mg/kg thymoquinone. Serum lipid hydroperoxide (LOOH) and total free sulfhydryl (Sh) levels were determined. Light microscopy was used to evaluate histological changes in brain tissue.RESULTS: Serum LOOH levels (0.21± 0.04 for control group, 0.29 ± 0.01 for sham group, 0.23 ± 0.09 for silymarin group, 0.29 ± 0.09 for thymoquinone group) were significantly higher and Sh levels (10.74 ± 1.71 for control group, 6.82 ± 0.24 for sham group, 9.12 ± 1.04 for silymarin group, 8.41 ± 1.12 for thymoquinone group)were significantly lower in control, silymarin and thymoquinone groups compared to control group (p

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PMID: 

Cancer Chemother Pharmacol. 2019 Dec 12. Epub 2019 Dec 12. PMID: 31832810

Abstract Title: 

6-Gingerol induces cell-cycle G1-phase arrest through AKT-GSK 3β-cyclin D1 pathway in renal-cell carcinoma.

Abstract: 

PURPOSE: 6-Gingerol, a major biochemical and pharmacological active ingredient of ginger, has shown anti-inflammatory and antitumor activities against various cancers. Searching for natural products with fewer side effects for developing adjunctive therapeutic options is necessary.METHODS: The effects of 6-gingerol on proliferation, colony formation, and cell cycle in RCC cells were detected by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony formation assay, and propidium iodide (PI) staining, respectively. Western blotting, an immunofluorescence assay, and immunohistochemical staining were performed to assess the expression of relevant proteins. A subcutaneous tumor model was set up to investigate the 6-gingerol effects on tumor growth in vivo, and the pharmacokinetics of 6-gingerol in mice were detected by LC/MS assays.RESULTS: 6-Gingerol treatment exerted time- and dose-dependent inhibition of the growth and colony formation of ACHN, 786-O, and 769-P cells, leading to a concomitant induction of cell-cycle G1-phase arrest and decrease in Ki-67 expression in the cell nucleus. Western-blotting results showed that 6-gingerol reduces phosphorylation of protein kinase B (AKT) Ser 473, cyclin-dependent kinases (CDK4), and cyclin D1 and, meanwhile, increases glycogen synthase kinase (GSK 3β) protein amount. Furthermore, the efficacy of 6-gingerol was demonstrated in an in vivo murine model of 786-O.CONCLUSION: The above results indicate that 6-gingerol can induce cell-cycle arrest and cell-growth inhibition through the AKT-GSK 3β-cyclin D1 signaling pathway in vitro and in vivo, suggesting that 6-gingerol should be useful for renal-cell carcinoma treatment.

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PMID: 

Adv Pharm Bull. 2019 Oct ;9(4):685-689. Epub 2019 Oct 24. PMID: 31857975

Abstract Title: 

10-Gingerol Inhibits Ovarian Cancer Cell Growth by Inducing G2 Arrest.

Abstract: 

Gingerol homologs found in the rhizomes of ginger plants have the potential to benefit human health, including the prevention and treatment of cancer. This study evaluated the effect of 10-gingerol on ovarian cancer cell (HEY, OVCAR3, and SKOV-3) growth.Cell growth was measured by MTT assays, flow cytometry was used to assess cell proliferation, cytotoxicity and cell cycle progression, and western blotting was used to measure cyclin protein expression.Ovarian cancer cells that were treated with 10-gingerol experienced a time- and dose-dependent decrease in cell number, which was due to a reduction in cell proliferation rather than a cytotoxic effect. Reduced proliferation of 10-gingerol-treated ovarian cancer cells was associated with an increased percentage of cells in G2 phase of the cell cycle and a corresponding reduction in the percentage of cells in G1. Ovarian cancer cells also showed decreased cyclin A, B1, and D3 expression following exposure to 10-gingerol.These findings revealed that 10-gingerol caused a G2 arrest-associated suppression of ovarian cancer cell growth, which may be exploited in the management of ovarian cancer.

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PMID: 

Nutrients. 2019 Dec 30 ;12(1). Epub 2019 Dec 30. PMID: 31905849

Abstract Title: 

The Influence of Lycopene, [6]-Gingerol, and Silymarin on the Apoptosis on U-118MG Glioblastoma Cells In Vitro Model.

Abstract: 

BACKGROUND: Lycopene, gingerol, and silymarin have a potential anticancer activity in many types of neoplasms. Healthy lifestyle and proper diet are associated with a reduced risk of cancer and other diseases. Increasingly, clinical research focuses on the mechanisms of action of natural compounds and their impact on the development of cancer. The aim of the present study was to determine the effect of lycopene, gingerol, and silymarin on apoptosis, mitochondrial potential and caspase-3/7 activity in the U118-MG cell line.METHODS: Human glioblastoma cells were incubated with lycopene, [6]-gingerol, and silymarin for 24 and 48 h. Apoptosis was monitored using the Annexin V labelling, caspase-3/7 activity, and early hallmark of apoptosis were determined with mitochondrial membrane potential changes.RESULTS: Our data showed a significant decrease in the viability glioblastoma cells U118-MG after 48 h treatment with lycopene, [6]-gingerol, and silymarin.CONCLUSIONS: Our data could confirm the stimulative effects of used compounds on apoptosis and changes in mitochondrial potential in a dose-dependent manner.

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