Quercetin protects human granulosa cells against oxidative stress via thioredoxin system

Granulosa Cells (GCs) are sensitive to excessive production of reactive oxygen species (ROS). Quercetin (QUR) is a free radical scavenger which can alleviate oxidative stress through nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/antioxidant response element (ARE) pathway and thioredoxin (Trx) system. We aimed to explore the probable protective role of QUR on cultured human GCs treated with hydrogen peroxide (H₂O₂) as an inducer of oxidative stress. MTT assay was applied for evaluating the cell cytotoxicity of QUR and H₂O₂. The rate of apoptotic cells and intracellular ROS generation were determined by Annexin V-FITC/PI staining and 2′-7′-dichlorodihydro?uorescein diacetate ?uorescent probes (DCFH-DA), respectively. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis and western blot analysis were used to evaluate the gene and protein expression of Nrf2 and kelch-like ech-associated protein 1 (Keap1)1. The Nrf2 and Trx activities were measured by Enzyme-linked Immunosorbent Assay (ELISA). The results indicated that QUR pretreatment can decrease ROS production and apoptosis induced by H₂O₂. In addition, QUR increased Nrf2 gene and protein expression, as well as its nuclear translocation. Moreover, in QUR-treated group, a lower level of Keap1 protein was observed, which was not reported as significant. The results also indicated a significant correlation between the expression of Nrf2 and Keap1 in QUR-treated group. Further, QUR protected GCs from oxidative stress by increasing Trx gene expression and activity. This study suggests that QUR as a supplementary factor may protect GCs from oxidative stress in diseases related to this condition.     

Effect of Probiotics Bacillus coagulans and Lactobacillus plantarum on Lipid Profile and Feces Bacteria of Rats Fed Cholesterol-Enriched Diet

Probiotics and Antimicrobial Proteins - The aim of this study was to investigate the effect of Lactobacillus plantarum and Bacillus coagulans on serum lipid profile and lowering potential of...     

Ethanol-induced impairment of polyamine homeostasis – A potential cause of neural tube defect and intrauterine growth restriction in fetal alcohol syndrome

Introduction

Polyamines play a fundamental role during embryogenesis by regulating cell growth and proliferation and by interacting with RNA, DNA and protein. The polyamine pools are regulated by metabolism and uptake from exogenous sources. The use of certain inhibitors of polyamine synthesis causes similar defects to those seen in alcohol exposure e.g. retarded embryo growth and endothelial cell sprouting.

Methods

CD-1 mice received two intraperitoneal injections of 3 g/kg ethanol at 4 h intervals 8.75 days post coitum (dpc). The fetal head, trunk, yolk sac and placenta were collected at 9.5 and 12.5 dpc and polyamine concentrations were determined.

Results

No measurable quantity of polyamines could be detected in the embryo head at 9.5 dpc, 12 h after ethanol exposure. Putrescine was not detectable in the trunk of the embryo at that time, whereas polyamines in yolk sac and placenta were at control level. Polyamine deficiency was associated with slow cell growth, reduction in endothelial cell sprouting, an altered pattern of blood vessel network formation and consequently retarded migration of neural crest cells and growth restriction.

Discussion

Our results indicate that the polyamine pools in embryonic and extraembryonic tissues are developmentally regulated. Alcohol administration, at the critical stage, perturbs polyamine levels with various patterns, depending on the tissue and its developmental stage. The total absence of polyamines in the embryo head at 9.5 dpc may explain why this stage is so vulnerable to the development of neural tube defect, and growth restriction, the findings previously observed in fetal alcohol syndrome.     

Morphological and molecular genetic variations of oat genotypes grown in Kermanshah,Iran

Morphological traits and molecular markers are two common methods for genetic variation studies. Molecular markers, morphological traits methods and relationship between the two were used to study genetic variation among 43 oat genotypes and varieties. For this purpose, an augmented design was conducted in three replicates at 2008–2009 cropping season in the experimental field of Campus of Agriculture and Natural Resources of Razi University, Kermanshah, Iran. Four wild oat accessions (Avena sterilis) were added to evaluated genotypes in molecular experiment. Results showed a significant variation among genotypes for all morphological traits and they were classified based on this variation in four groups by WARD cluster analysis. In molecular experiment, 28 inter simple sequence repeat (ISSR) primers amplified 206 polymorph bands. Based on Jaccard similarity matrix, similarity among genotypes was varied from 0.23 to 0.66 and cluster analysis classified genotypes in seven groups by complete linkage method. The correlation between ISSR marker and morphological traits classifications was not significant. ISSR showed to be a helpful marker for genotype identity and separation as it put wild accessions in a group.     

Alternatives to key factor analyses for assessing the population dynamics of Hypera postica (Coleoptera: Curculionidae)

Key factors are those causes that are most responsible for the observed changes in population density between generations. Stage-frequency of alfalfa weevil was modeled using Manly-1997 model. Multiple decrement life table parameters from an 8 year-field study were analyzed using traditional and λ contribution methods. In traditional method, the key factor was determined as k _LII, the death of period-two larvae from all mortality factors, whereas in λ contribution method, the key factor was determined as b _2&3, oviposition rate of females per square meter. These differences result directly from the sensitivity of the population growth rate, λ, to variation of both k and b in various stages of the weevil. Among all mortality factors, only k _LI-Z, the death of period-one larvae from the entomopathogenic fungus, Zoophthora phytonomi (Arthur) Batko (Zygomycetes: Entomophthoraceae), k _LII and k _LII-Z, the death of period-two larvae from Z. phytonomi, acted in a density dependent fashion. Remaining factors were independent of population densities affected. Using λ contribution method, life table approach still remains a major way of studying the dynamics of field populations for applied ecologists and population managers.     

Prey preference and consumption capacity of Nephus arcuatus (Coleoptera: Coccinellidae): the influence of prey stage,prey size and feeding experience

This study examined the feeding habits of Nephus arcuatus Kapur (Coleoptera: Coccinellidae), an important predator of mealybugs in south-western Iran. The consumption capacity of male and female N. arcuatus adults was determined by their feeding on eggs, first-instar nymphs, and adult females of two destructive mealybugs, Nipaecoccus viridis (Newstead) and Planococcus citri Risso, over a 24-h period. N arcuatus consumed significantly more first-instar nymphs than eggs, and more eggs than female adults of both prey species. In addition, we also studied the developmental stage prey preference of adults reared on either N. viridis or P. citri and found that the prey preference of females did not change with the developmental stage of the mealybug. Meanwhile, the males reared on either N. viridis or P. citri showed a significant preference for the first-instar nymphs of P. citri over first-instar nymphs of N. viridis, while a preference for the eggs or adult females of these two mealybugs was not observed. This selection of first-instar nymphs by males was not tied to its previous feeding experience. Our findings suggest that prey stage, prey size and previous feeding experience had no effect on the prey selection of N. arcuatus, making it a good candidate for the biological control of mealybugs.     

S100A8/9 induces cell death via a novel, RAGE-independent pathway that involves selective release of Smac/DIABLO and Omi/HtrA2

A complex of two S100 EF-hand calcium-binding proteins S100A8/A9 induces apoptosis in various cells, especially tumor cells. Using several cell lines, we have shown that S100A8/A9-induced cell death is not mediated by the receptor for advanced glycation endproducts (RAGE), a receptor previously demonstrated to engage S100 proteins. Investigation of cell lines either deficient in, or over-expressing components of the death signaling machinery provided insight into the S100A8/A9-mediated cell death pathway. Treatment of cells with S100A8/A9 caused a rapid decrease in the mitochondrial membrane potential (DeltaPsi(m)) and activated Bak, but did not cause release of apoptosis-inducing factor (AIF), endonuclease G (Endo G) or cytochrome c. However, both Smac/DIABLO and Omi/HtrA2 were selectively released into the cytoplasm concomitantly with a decrease in Drp1 expression, which inhibits mitochondrial fission machinery. S100A8/A9 treatment also resulted in decreased expression of the anti-apoptotic proteins Bcl2 and Bcl-X(L), whereas expression of the pro-apoptotic proteins Bax, Bad and BNIP3 was not altered. Over-expression of Bcl2 partially reversed the cytotoxicity of S100A8/A9. Together, these data indicate that S100A8/A9-induced cell death involves Bak, selective release of Smac/DIABLO and Omi/HtrA2 from mitochondria, and modulation of the balance between pro- and anti-apoptotic proteins.     

β-catenin and transforming growth factor β have distinct roles regulating fibroblast cell motility and the induction of collagen lattice contraction

Background  

β-catenin and transforming growth factor β signaling are activated in fibroblasts during wound healing. Both signaling pathways positively regulate fibroblast proliferation during this reparative process, and the effect of transforming growth factor β is partially mediated by β-catenin. Other cellular processes, such as cell motility and the induction of extracellular matrix contraction, also play important roles during wound repair. We examined the function of β-catenin and its interaction with transforming growth factor β in cell motility and the induction of collagen lattice contraction.