Gustavsenbarnes2380

Apelin was thought to be an adipocyte-specific hormone, but recent studies have indicated a link between apelin and placenta function e.g. cell proliferation. The aim of the study was investigating dose- and time-dependent effect of apelin on hormone secretion including steroids progesterone (P4) and estradiol (E2) and proteins chorionic gonadotropin (hCG), human placental lactogen (hPL), placental growth factor (PLGF), as well as protein expression of steroid enzymes (3βHSD, CYP19) and protein hormones (hCG, hPL and PLGF) in placental cells. Syncytiotrophoblast BeWo cells, as human trophoblast models, were treated for 24, 48, and 72 hours with the human recombinant apelin at doses 0.02, 0.2, 2.0, 20 and 200 ng/ml followed by culture medium. Concentrations of the above hormones were studied by ELISA kits. learn more Furthermore, protein expression of steroid enzymes and protein hormones were measured using Western blot. Our results showed that apelin significantly decreased both steroid and protein hormones by inhibiting steroid enzymes or protein hormone expression. Moreover, we demonstrated that apelin at dose 2.0 ng/ml increased phosphorylation of protein kinase A (PKA) from 1 to 60 min of BeWo cell incubation. Inhibitory effect of apelin on P4, E2 and PLGF secretion were abolished when BeWo cells were cultured in the presence of ML221, an apelin receptor antagonist, PD98059, an extracellular signal-regulated kinases (ERK1/2) antagonist and KT5720, a PKA antagonist. In turn, secretion of hCG and hPL occurs only in the presence of ML221 and PD98059. In conclusion, our results indicate that apelin can be considered as a gestational hormone implied in the endocrine function of the human placenta, with an important role in controlling the production of steroid and protein hormones in placental BeWo cells.Cyclosporine A (CsA) is an immunosuppressive drug used in transplantation and treatment of autoimmune diseases. Experimental studies revealed impairments in liver function and morphology among cyclosporine-treated animals. The aim of the study was to evaluate hepatoprotective activity of peroxisome-proliferator-activated receptors γ (PPARγ) ligands rosiglitazone and 15-deoxy-Δ12,14-prostaglandin J2 (PGDJ2) on CsA-induced hepatotoxicity in experimental animals. CsA was administered subcutaneously at a dose of 15 mg/kg/day for 28 days. Both PPARγ agonists were given for 28 days 0.5 hour before the administration of CsA. Rosiglitazone was administered orally at a dose of 8 mg/kg/day and PGDJ2 was given intraperitoneally at a dose of 30 μg/kg/day. CsA induced liver injury was evidenced by increased serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and bilirubin. Concentrations of glutathione (GSH) and glutathione disulfide (GSSG), lipid peroxidation products, nicotinamide adenine dinucleotide+/nicotinamide adenine dinucleotide hydrogen (NAD+/NADH), nicotinamide adenine dinucleotide phosphate+/nicotinamide adenine dinucleotide phosphate hydrogen (NADP+/NADPH) and adenosine diphosphate/adenosine triphosphate (ADP/ATP) ratios and caspase 3 activity that were measured in the liver tissue showed, that CsA induced oxidative stress, evoked an imbalanced redox state and apoptosis in the liver. Microscope examination showed sinusoidal dilatation, mononuclear cell infiltration, necrosis of hepatocytes, intracellular vacuolar degeneration and microvesicular steatosis and apoptopic cells. The biochemical and morphological changes induced by CsA were limited by administration of both PPARγ agonist - rosiglitazone and PGDJ2. Our biochemical and liver histopathological examination indicate that both PPARγ agonists may play an important role in protecting against CsA-induced hepatotoxicity.The preconditioning effect of a mild stressor can reduce the ulcerogenic effect of a severe stressor on the gastric mucosa. The aim of the study was to investigate the effect of preconditioning stress on the gastric and the small intestinal injury caused by a single injection of indomethacin (IM) in conscious rats. Preliminary fasting (24 hours) rats were subjected IM administration (35 mg/kg, subcutaneously) with preconditioning stress (30 min cold-restraint at 10°C and further 1 hour keeping in cages at room temperature) or without stress. Plasma corticosterone level, heart rate (HR), blood pressure (BP) and somatic pain sensitivity (tail flick latency) were measured under circumstances of the gastrointestinal IM-induced injury in preliminary stressed and non-stressed rats. IM administration induced formation of gastric erosions well visible 4 hours after its injection. The healing of gastric erosions for 48 hours was accompanied by the development of a small intestinal injury. Corticosterone levels were el mucosa to ulcerogenic action of IM, stabilizes the hemodynamic parameters and normalizes somatic pain sensitivity.The aim of the research was to assess the effect of nesfatin-1 on the structure, flexibility parameters, and expression of adropin, nesfatin-1, and angiotensin II receptor type 1 (AT1R) in the abdominal aorta in ovariectomized rats. Fragments of aortas were collected after euthanasia of female sham-operated (CONT) and ovariectomized Wistar rats (EXP), which were administered intraperitoneal injection of physiological saline (CONT, n = 7; EXP-O, n = 7) or nesfatin-1 (EXP-N, n = 7) in an amount of 2 μg/kg b.w. once a day for 8 weeks. The samples of aortas were collected for measurement of elasticity as well as histomorphometric, immunohistochemical, FTIR, and Raman spectroscopy analysis. The ovariectomy caused a significant increase in the thickness of the total wall and its particular layers in the aorta, in comparison to the CONT and EXP-N groups. However, the ovariectomy led to a decrease in the amount of elastin, collagen (mature, immature collagen, collagen maturity ratio 1660 - 1690 cm-1), and amides, with a simultaneous increase in lipids, especially in the tunica intima-media of the abdominal aorta compared to the other groups. The use of nesfatin-1 significantly increased the amount of collagen, elastin and amides with a simultaneous decrease in the amount of lipids and the expression of AT1R, adropin and nesfatin-1 in the abdominal aorta of ovariectomized rats. In conclusion, our study showed that the ovariectomy surgery induced changes in the abdominal aorta wall characteristic for aging females. Application of nesfatin-1 may prevent the negative consequences in the vessel wall structure in females in conditions of estrogen deficiency and prevent atherosclerotic changes in the cardiovascular system.