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Prostaglandin E2 Levels (prostaglandin + e2_level)

Distribution by Scientific Domains

Medical Sciences	80%

Selected Abstracts

Effect of chemical peeling on photocarcinogenesis

THE JOURNAL OF DERMATOLOGY, Issue 10 2010
Mohamed ABDEL-DAIM
Abstract Chemical peeling is one of the dermatological treatments available for certain cutaneous diseases and conditions or improvement of cosmetic appearance of photo-aged skin. We assessed the photo-chemopreventive effect of several clinically used chemical peeling agents on the ultraviolet-irradiated skin of hairless mice. Chemical peeling was done using 35% glycolic acid dissolved in distilled water, 30% salicylic acid in ethanol, and 10% or 35% trichloroacetic acid in distilled water at the right back of ultraviolet-irradiated hairless mice every 2 weeks for glycolic acid, salicylic acid and 10% trichloroacetic acid, and every 4 weeks for 35% trichloroacetic acid for a total of 18 weeks after the establishment of photo-aged mice by irradiation with ultraviolet B range light three times a week for 14 weeks at a total dose of 6.66 J/cm2. Tumor formation was assessed every week. Skin specimens were taken from treated and non-treated area for evaluation under microscopy, evaluation of p53 expression and mRNA expression of cyclooxygenase-2. Serum level of prostaglandin E2 was also evaluated. All types of chemical peeling reduced tumor formation in treated mice, mostly in the treated area but also in the non-treated area. Peeling suppressed retention of p53-positive abnormal cells and reduced mRNA expression of cyclooxygenase-2 in treated skin. Further, serum prostaglandin E2 level was decreased in chemical peeling treated mice. These results indicate that chemical peeling with glycolic acid, salicylic acid and trichloroacetic acid could serve tumor prevention by removing photo-damaged cells. [source]

Role of phospholipases A2 in growth-dependent changes in prostaglandin release from 3T6 fibroblasts

JOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2001
Teresa Sánchez
Previously, we reported a growth-dependent change in prostaglandin production as a consequence of a marked growth-dependent alteration in arachidonic acid (AA) mobilization from phospholipids. Our present results show that fetal calf serum (FCS) and 4,-phorbol-12-myristate acetate (PMA) caused an enhancement of phospholipase A2 (PLA2) activity in the membrane fraction of non-confluent cells allowing PLA2 access to its substrate and the release of AA. Western blot analysis has shown that FCS and PMA increased secreted PLA2 (sPLA2) expression in non-confluent 3T6 fibroblast cultures. Moreover, FCS and PMA induced dithiothreitol-sensitive and bromoenol lactone-sensitive PLA2 activities in cytosol and membrane fraction. However, these stimuli did not modify significantly the PLA2 activity in both fractions when 3T6 fibroblasts reached a high cell density. This could be associated with the impairment of AA mobilization in these cell culture conditions. On the other hand, we observed that FCS and PMA induced the same prostaglandin H synthase-2 induction in non-confluent and confluent culture conditions. Moreover, the prostaglandin E2 levels reached in cell culture supernatants were independent of the degree of confluence when AA was added exogenously. These results suggest that the changes of intracellular distribution of PLA2 activity of sPLA2 and iPLA2 stimulated by exogenous stimuli may be controlled by cell density conditions which constitute an important mechanism in the regulation of prostaglandin release.© 2001 Wiley-Liss, Inc. [source]

Increased prostaglandin E2 levels in the airway of patients with eosinophilic bronchitis

ALLERGY, Issue 1 2008
B. Sastre
Background:, Eosinophilic bronchitis is a common cause of chronic cough, which like asthma is characterized by sputum eosinophilia, but unlike asthma there is no variable airflow obstruction or airway hyperresponsiveness. We tested the hypothesis that the different airway function in patients with eosinophilic bronchitis and asthma could be caused by an imbalance in the production of bronchoconstrictor (LTC4) and bronchoprotective (prostaglandin E2; PGE2) lipid mediators. Methods:, We measured cytokines levels, proinflammatory mediators and eicosanoids concentration in sputum from 13 subjects with nonasthmatic eosinophilic bronchitis, 13 subjects with asthma, and 11 healthy control subjects. Cytokines mRNA levels were measured by real time PCR, proinflammatory mediators, PGE2, and LTC4 were measured by enzyme immunoassays. Results:, The median sputum eosinophil count was not statistically different in patients with asthma (7.95%) and eosinophilic bronchitis (15.29%). The levels of mRNA specific to interleukin-5 (IL-5), IL-4, IL-10, IL-13, interferon , (IFN-,), IL-2, vascular endothelial growth factor and transforming growth factor , were similar in both conditions. In addition, no differences were found between asthma and eosinophilic bronchitis in proinflammatory cytokines, such as IL-8, IFN-, and tumor necrosis factor , (TNF-,) levels. Sputum cysteinyl-leukotrienes concentration was raised both in eosinophilic bronchitis and asthma patients. We found that induced sputum PGE2 concentrations were significantly increased in subjects with eosinophilic bronchitis (838.3 ± 612 pg/ml) when compared with asthmatic (7.54 ± 2.14 pg/ml) and healthy subjects (4 ± 1.3 pg/ml). Conclusion:, This data suggest that the difference in airway function observed in subjects with eosinophilic bronchitis and asthma could be due to differences in PGE2 production in the airways. [source]

Effect of systemic administration of nicotine on healing in osseous defects.

CLINICAL ORAL IMPLANTS RESEARCH, Issue 5 2006
An experimental study in rabbits.
Abstract Objectives: The aim of the present study was to analyze the effect of systemic administration of nicotine on bone healing in osseous defects in the tibia of rabbits. Material and methods: Sixteen female rabbits received nicotine (n=8; test group) or saline (n=8; control group) via subcutaneously placed mini-osmotic pumps for 8 weeks. The animals underwent three surgical operations during the experimental period, and body weight was registered weekly. Blood samples were collected to determine cotinine and prostaglandin E2 levels. Bone preparations were made in the right leg of all rabbits after 4 weeks and in the left leg after 6 weeks of nicotine/placebo exposure. Thus, 2- and 4-week healing groups were created for the bone defects. After 8 weeks, the animals were killed. Tissue blocks including the bone defects were prepared for histological analysis. Results: The animals in the test group lost weight, while the control group gained weight during the experiment. The prostaglandin E2 levels in plasma increased significantly following nicotine exposure in the test group. No significant differences in the percentage of vessels and bone density in the osseous defects were found between the test and the control groups after 2 and 4 weeks of healing. Conclusions: In this experiment, systemic administration of nicotine over 4 or 6 weeks, respectively, influenced body weight and systemic prostaglandin E2 levels but not the amount of blood vessels and the bone mineral density in bone defects after 2 or 4 weeks of healing. [source]