Effects of Glucocorticoids and Progesterone on Prostaglandin E2 and Leukotriene B4 Release by Human Fetal Membranes at Term Gestation

Zicari, Alessandra; Ticconi, Carlo; Pontieri, G. M.; Loyola, Giovanni; Piccione, Emilio

doi:10.1016/s0090-6980(97)00124-x

Cited by 10 publications

(4 citation statements)

References 19 publications

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“…Previous studies have shown that GCs are a strong inhibitor of the arachidonic acid cascade, resulting in less production of prostaglandin E2 (PGE2) in macrophages, vascular smooth muscle cells, and MSCs ( 27 – 30 ). In addition, other studies have suggested that the expression of CXCR4 is elevated in the presence of PGE2 ( 31 ).…”

Section: Resultsmentioning

confidence: 99%

Glucocorticoid Impaired the Wound Healing Ability of Endothelial Progenitor Cells by Reducing the Expression of CXCR4 in the PGE2 Pathway

et al. 2018

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Background: Endothelial progenitor cells (EPCs) can be used to treat ischemic disease in cell-based therapy owing to their neovascularization potential. Glucocorticoids (GCs) have been widely used as strong anti-inflammatory reagents. However, despite their beneficial effects, side effects, such as impairing wound healing are commonly reported with GC-based therapy, and the effects of GC therapy on the wound healing function of EPCs are unclear.Methods: In this study, we investigated how GC treatment affects the characteristics and wound healing function of EPCs.Results: We found that GC treatment reduced the proliferative ability of EPCs. In addition, the expression of CXCR4 was dramatically impaired, which suppressed the migration of EPCs. A transplantation study in a flap mouse model revealed that GC-treated EPCs showed a poor homing ability to injured sites and a low activity for recruiting inflammatory cells, which led to wound healing dysfunction. Impairment of prostaglandin E2 (PGE2) synthases, cyclooxygenase (COX2) and microsomal PGE2 synthase 1 (mPEGS1) were identified as being involved in the GC-induced impairment of the CXCR4 expression in EPCs. Treatment with PGE2 rescued the expression of CXCR4 and restored the migration ability of GC-treated EPCs. In addition, the PGE2 signal that activated the PI3K/AKT pathway was identified to be involved in the regulation of CXCR4 in EPCs under the effects of GCs. In addition, similar negative effects of GCs were observed in EPCs under hypoxic conditions. Under hypoxic conditions, GCs independently impaired the PGE2 and HIF2α pathways, which downregulated the expression of CXCR4 in EPCs. Our findings highlighted the influences of GCs on the characteristics and functions of EPCs, suggesting that the use of EPCs for autologous cell transplantation in patients who have used GCs for a long time should be considered carefully.

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Section: Resultsmentioning

confidence: 99%

Glucocorticoid Impaired the Wound Healing Ability of Endothelial Progenitor Cells by Reducing the Expression of CXCR4 in the PGE2 Pathway

et al. 2018

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“…Betamethasone is a synthetic glucocorticoid possessing anti-inflammatory [1] and antiallergic properties [2]. It works by affecting the synthesis of prostaglandin [3] and leukotriene [4]. Dexchlorpheniramine, usually used in form of maleate salt, is the pharmacologically active dextrorotatory enantiomer of chlorpheniramine [5], an antihistamine working on H1 receptors to reduce the allergic reactions [6].…”

Section: Introductionmentioning

confidence: 99%

Simultaneous Assay of Dexchlorpheniramine Maleate, Betamethasone, and Sodium Benzoate in Syrup by a Reliable and Robust HPLC Method

Ngo

2019

Journal of Analytical Methods in Chemistry

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The simultaneous determination of betamethasone, dexchlorpheniramine maleate, and sodium benzoate in pharmaceutical syrup was done by using a simple validated HPLC method. The chromatographic separation of the three analytes was done in a C18 column maintained at 25°C, using a mixture of acetonitrile and 0.02 M phosphate buffer solution pH 2.70 (35 : 65, v : v) as mobile phase. The isocratic elution was chosen with total flow rate of mobile phase maintained at 1.0 mL per minute. The analytes were detected by a UV-Vis detector set at 254 nm. Injection volume was set at 50 μl. The method was fully validated in terms of specificity, linearity, precision, accuracy, and robustness according to requirements of current guidelines and was proven to be suitable for the intended application.

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“…In rats exposed to behavioral stress (i.e., maternal separation) and chronically provided dietary n-3 PUFA, corticosterone was reduced associated with modest reductions in PGE 2 , suggesting that reduced prostaglandin synthesis was independent of elevated GCs (44) and contrary to the lipocortin theory of glucocorticoid suppression of prostaglandins (45). In addition, GCs had no effect on PGE 2 secretion but substantially increased leukotriene B4 (LTB 4 ), suggesting that elevated GCs had no effect on prostaglandin synthesis but did stimulate LOX-mediated oxylipins in human fetal membranes (46). In the present study, fasting-associated increase in cortisol (1) was associated with reductions of nearly twofold in PGF 2a and fivefold in TXB 2 , suggesting that GCs suppress prostaglandin and thromboxane synthesis and consistent with most in vivo data (47).…”

Section: Discussionmentioning

confidence: 96%

Oxylipin responses to fasting and insulin infusion in a large mammalian model of fasting-induced insulin resistance, the northern elephant seal

Wright

Katundu

Viscarra

et al. 2021

American Journal of Physiology-Regulatory, Integrative and Comp

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The prolonged, post-weaning fast of northern elephant seal (Mirounga angustirostris) pups is characterized by a reliance on lipid metabolism and reversible, fasting-induced insulin resistance providing a unique model to examine the effects of insulin on lipid metabolism. We have previously shown that acute insulin infusion induced a shift in fatty acid metabolism dependent on fasting duration. This study complements the previous study by examining the effects of fasting duration and insulin infusion on circulating levels of oxylipins, bioactive metabolites derived from the oxygenation of polyunsaturated fatty acids. Northern elephant seal pups were studied at two post-weaning periods (n = 5/period): early fasting (1-2 weeks post-weaning; 127 ± 1 kg) and late fasting (6-7 weeks post-weaning; 93 ± 4 kg). Different cohorts of pups were weighed, sedated, and infused with 65 mU/kg of insulin. Plasma was collected prior to infusion (T0), and at 10, 30, 60, and 120 min post-infusion. A profile of ~80 oxylipins were analyzed by UPLC-ESI-MS/MS. Nine oxylipins changed between early and late fasting and eight were altered in response to insulin infusion. Fasting decreased PGF2a and increased 14,15-DiHETrE, 20-HETE, and 4-HDoHE (p<0.03) in T0 samples, while insulin infusion resulted in an inverse change in area under the curve (AUC) levels in these same metabolites (p<0.05). In addition, 12-HpETE and 12-HETE decreased with fasting and insulin infusion, respectively (p<0.04). The oxylipins altered during fasting and in response to insulin infusion may contribute to the manifestation of insulin resistance and participate in the metabolic regulation of associated cellular processes.

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Effects of Glucocorticoids and Progesterone on Prostaglandin E2 and Leukotriene B4 Release by Human Fetal Membranes at Term Gestation

Cited by 10 publications

References 19 publications

Glucocorticoid Impaired the Wound Healing Ability of Endothelial Progenitor Cells by Reducing the Expression of CXCR4 in the PGE2 Pathway

Glucocorticoid Impaired the Wound Healing Ability of Endothelial Progenitor Cells by Reducing the Expression of CXCR4 in the PGE2 Pathway

Simultaneous Assay of Dexchlorpheniramine Maleate, Betamethasone, and Sodium Benzoate in Syrup by a Reliable and Robust HPLC Method

Oxylipin responses to fasting and insulin infusion in a large mammalian model of fasting-induced insulin resistance, the northern elephant seal

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