15 research outputs found
Influence of LPS on cell viability.
<p>U937 cell were exposed to 10 µg/mL of LPS for 24 h and cell viability was assessed by MTT assay. Results are expressed in percentage of control (mean ± SEM of five independent experiments, performed in triplicate). *p<0.05 vs control cells (0 µg/mL of LPS); **p<0.01 vs control cells.</p
Effect of ASTA on expression of Nrf2.
<p>U937 cells were treated with LPS or ASTA at the doses indicated. Groups include the following: Nuclear, Nrf2 protein levels in nuclear extracts; Cytosolic, Nrf2 protein levels in cytosolic fractions; panels on left show results of Western blot as appropriate. Plot on right shows the results of quantitative analysis. *<i>p</i><0.05 compared with control cells; <sup>§</sup><i>p</i><0.05 compared with LPS-treated cells.</p
Effect of ASTA on expression and activity of HO-1.
<p>A) Western blot and quantitative analysis for HO-1 expression, actin being used as loading control; data shown are means ± SD, *<i>p</i><0.05 compared with control cells; <sup>§</sup><i>p</i><0.05 compared with LPS or ASTA treated cells; data were from at least three independent experiments, each performed in triplicate. B) Mean HO activity (nmol/bilirubin/mg protein)/h ± SD, n = 3) detectable in homogenates obtained from U937 cells: untreated; treated with LPS, ASTA and LPS+ASTA. *<i>p</i><0.05 compared with control cells; <sup>§</sup><i>p</i><0.05 compared with LPS or ASTA treated cells.</p
The effect of HO-1 inhibition and ASTA treatment on cellular superoxide anion release.
<p>Values are means±SD of values from three experiments. The control value (no addition of ASTA) was set at 1. *p<0.05 vs control cells; <sup>§</sup>p<0.05 vs. LPS treated cells.</p
Effects of ASTA on viability of U937 cells.
<p>Cells were incubated with or without ASTA (10 µM) for 1 h, and then stimulated with LPS (10 µg/ml) for another 24 h. Cell viability was determined as described in the Materials and Methods section. Data are the mean values of three experiments ± SEM. *p<0.05 vs. control cells; <sup>§</sup>p<0.05 vs. LPS or ASTA treated cells.</p
Effect of ASTA treatment on superoxide anion generation assessed by estimating reduced nitrobluetetrazolium (NBT) inU937 cells.
<p>O<sub>2</sub><sup>−</sup> production increased significantly in U937 cells stimulated with LPS. ASTA blocked LPS-induced O<sub>2</sub><sup>−</sup> production. Values are means±SD of values from three experiments. The control value (no addition of ASTA) was set at 1. *p<0.05 vs control cells; <sup>§</sup>p<0.05 vs. LPS or ASTA treated cells.</p
mTOR Activation by PI3K/Akt and ERK Signaling in Short ELF-EMF Exposed Human Keratinocytes
<div><p>Several reports suggest that ELF-EMF exposures interact with biological processes including promotion of cell proliferation. However, the molecular mechanisms by which ELF-EMF controls cell growth are not completely understood. The present study aimed to investigate the effect of ELF-EMF on keratinocytes proliferation and molecular mechanisms involved. Effect of ELF-EMF (50 Hz, 1 mT) on HaCaT cell cycle and cells growth and viability was monitored by FACS analysis and BrdU assay. Gene expression profile by microarray and qRT-PCR validation was performed in HaCaT cells exposed or not to ELF-EMF. mTOR, Akt and MAPKs expressions were evaluated by Western blot analysis. In HaCaT cells, short ELF-EMF exposure modulates distinct patterns of gene expression involved in cell proliferation and in the cell cycle. mTOR activation resulted the main molecular target of ELF-EMF on HaCaT cells. Our data showed the increase of the canonical pathway of mTOR regulation (PI3K/Akt) and activation of ERK signaling pathways. Our results indicate that ELF-EMF selectively modulated the expression of multiple genes related to pivotal biological processes and functions that play a key role in physio-pathological mechanisms such as wound healing.</p></div
Associations between the Antioxidant Network and Emotional Intelligence: A Preliminary Study
<div><p>Background</p><p>Emotional intelligence (EI) can be broadly defined as the ability to cope with environmental demands. In the scientific research, however, there is not a univocal precise definition of EI and recent articles have underlined the necessity to explore its biological basis to advance understanding of the construct. The aim of study was to investigate if the antioxidant network may be associated with typical-performance or trait EI.</p><p>Methods</p><p>The study group consisted of 50 women (age, M = 25.10, SD = 3.87). Super Oxide Dismutase (SOD), Catalase (CAT), Glutathione Reductase (GR), and Glutathione Peroxidase (GPx) activities were evaluated on proteins extracted from Peripheral Blood Mononuclear Cells. Participants completed the Italian version of the EQ-i (Bar-On, 1997) as a measure of trait EI.</p><p>Results</p><p>We observed positive and significant correlations between some biological variables and EQ-i scores, and a significant predictive effect of CAT activity when controlling for related biological variables, age, and smoking.</p><p>Conclusions</p><p>Our preliminary study suggests that the antioxidant network may constitute some of trait EI's biological basis. In particular, CAT and the SOD/CAT ratio could be two biological variables involved in some specific components of EI.</p></div
Effects of pharmacological inhibitors on HaCaT cells proliferation.
<p>Proliferative rate of HaCaT cells assed by BrdU incorporation assay, after 24 h of incubation in non-exposed and exposed to ELF-EMF only for the first hour. Cells were pre-treated or not with selective inhibitor of ERK kinase activity (PD980559, 1 μM), PI3K (Ly294002, 1 μM), JNK Inhibitor II (20 μM) for 30 min. Each bar represents the mean±SD of three independent experiments performed in triplicate.</p
Effect of ELF-EMF exposure on AKT and MAPK activity.
<p>A. Representative image of immunoblotting for p-ERK, p-JNK, p-p38 and p-AKT of gels using three separate pools of protein extracted from HaCaT cells time-course exposed to ELF-EMF. B. Averaged band density of p-ERK, p-JNK, p-p38-immunoreactive and p-AKT is expressed as relative expression in both exposed and non-exposed to ELF-EMF (mean±SD; <sup>#</sup><i>p<0</i>.<i>05 vs</i> time related non-exposed cells).</p