No abstract available.
Amnion* ; Dinoprostone* ; Humans* ; Metabolism*

No abstract available.
Amnion* ; Dinoprostone* ; Humans* ; Metabolism* ; Progesterone*

No abstract available.
Amnion* ; Dinoprostone* ; Humans* ; Metabolism* ; Progesterone*

OBJECTIVETo determine the concentrations of interleukin-18 (IL-18), IL-6, IL-8, and prostaglandin E2 (PGE2) in the synovial fluid in patients with osteoarthritis (OA), and explore the role of IL-18 in the pathogenesis of OA.

METHODSThe synovial fluid was collected from 30 patients with knee OA, and the concentrations of IL-18 and the other cytokines were measured using enzyme-linked immunosorbent assay (ELISA). A linear regression was performed between IL-18 and the other cytokines.

RESULTSThe average IL-18 and PGE2 concentrations were 220-/+304 pg/ml and 89-/+104 pg/ml in the synovial fluid, respectively, and the two cytokines showed a positive correlation in the synovial fluid (r=0.628, P=0.001). The IL-18 concentration was also correlated to the concentrations of IL-6 (1200-/+1587 pg/ml, n=22; r=0.590, P=0.008) and IL-8 (5190-/+6024 pg/ml, n=9; r=0.776, P=0.014).

CONCLUSIONIL-18 can promote PGE2 production, which causes cartilage degradation in OA, thus therapies targeting this cytokine may prove an effective approach to early OA treatment.

Aged ; Dinoprostone ; biosynthesis ; Female ; Humans ; Interleukin-18 ; metabolism ; Male ; Middle Aged ; Osteoarthritis ; metabolism ; Synovial Fluid ; metabolism

Erythrocytes are devoid of nuclei and mitochondria which are the crucial elements of apoptosis, so their programmed suicidal death is called eryptosis. Eryptosis is characterized by cell shrinkage, membrane blebbing, activation of proteases, and phosphatidylserine exposure. Prostaglandin E(2) (PGE(2)) activates nonselective cation channels that increase cytosolic Ca(2+) activity and platelet-activating factor (PAF) activates a sphingomyelinase which lead to formation of ceramide. Either can lead to membrane scrambling with subsequent phosphatidylserine exposure. Exposed phosphatidylserine is recognized by macrophages that engulf and degrade the injured cells. As such, eryptosis can clear the injured red blood cells and avoid the release of hemoglobin. The signaling of eryptosis includes PGE(2), cation channels, PAF, ceramide, protein kinase C, and in some instances, caspases. In this review, the PGE(2), PAF and protein kinase pathways, erythrocyte surface receptor-mediated effects, oxidative stress and caspase effects, the inhibitory factors of eryptosis and the clinical eryptosis-related diseases are discussed.
Apoptosis ; physiology ; Dinoprostone ; metabolism ; Erythrocytes ; metabolism ; physiology ; Humans ; Platelet Activating Factor ; metabolism ; Signal Transduction

Prostaglandin E2 (PGE2), a bioactive lipid mediator, is one of the most important locally acting factors involved in a variety of physiological and pathophysiological processes. PGE2 binds with four EP receptors (EP1-4) to activate G protein-coupled receptor signaling responses. Recent functional and molecular studies have revealed that PGE2 plays an essential role in regulation of renal fluid transport via a variety of mechanisms. The water balance mainly depends on the regulation of aquaporin-2 (AQP2) by arginine vasopressin (AVP) in renal collecting duct principal cells. In recent years, increasing evidence suggests that PGE2 plays an important role in renal water reabsorption in the collecting ducts. In this paper, we reviewed the role of PGE2 and its receptors in the regulation of water reabsorption in the kidney, which may provide a new therapeutic strategy for many diseases especially nephrogenic diabetes insipidus.
Aquaporin 2/metabolism* ; Biological Transport ; Diabetes Insipidus, Nephrogenic ; Dinoprostone ; Humans ; Water/metabolism*

OBJECTIVE: To detect cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PGE2) release in human nasal epithelia (HNE) induced by lipopolysaccharide (LPS) in different concentration gradient and time gradient, and to investigate their roles in nasal inflammatory pathogenesis. METHOD: Western Blot and fluorescent real time quantitative PCR were performed to detect the expression of COX-2 in HNE induced by LPS and blocked by selective inhibitor of COX-2. The concentrations of PGE2 were determined by enzyme immunoassay. RESULT: Low expressions of COX-2 and PGE2 were detected in normal HNE. COX-2 expression and PGE2 release increased in HNE induced by LPS in time-dependent or dose-dependent manner. The increased release of PGE2 was later than that of COX-2 expression. COX-2 expression and PGE2 release were dose-dependently attenuated by selective inhibitor of COX-2. CONCLUSION LPS effectively induces COX-2 expression and PGE2 release in HNE. And COX-2 is responsible for the synthesis of PGE2. These results indicate that the increased expression of COX-2 and PGE2 is involved in the inflammation of HNE induced by LPS in vitro.
Cells, Cultured ; metabolism ; Cyclooxygenase 2 ; metabolism ; Dinoprostone ; biosynthesis ; metabolism ; Epithelial Cells ; metabolism ; Humans ; Lipopolysaccharides ; Nasal Mucosa ; cytology ; metabolism

AIM AND METHODSBoth PGE2 and cAMP are important neural mediator of fever. In order to discuss if PGE2 and cAMP are involved in the antipyretic mechanism of baicalin, fever models of rats were made by i.v. injection of endotoxin (ET). The antipyretic action and effects of baicalin on contents of PGE2 and cAMP in hypothalamus were observed.

RESULTSBaicalin possessed obvious antipyretic effect on fever rats and reversed the effect of ET on contents of PGE2 and cAMP in hypothalamus. Correlation analysis showed that contents of PGE2 and cAMP in hypothalamus were positively correlated with the change of body temperature of rats.

CONCLUSIONBaicalin may exert its antipyretic effect on fever rats by inhibiting increase of contents of PGE2 and cAMP in hypothalamus.

Animals ; Cyclic AMP ; metabolism ; Dinoprostone ; metabolism ; Fever ; metabolism ; Flavonoids ; pharmacology ; Hypothalamus ; drug effects ; metabolism ; Male ; Rats ; Rats, Wistar

OBJECTIVETo study the effects and the therapeutic mechanism of hyperbaric oxygen (HBO) on prostaglandin E(2) (PGE(2)) in alveolar bone and gingiva of experimental periodontitis in animal.

METHODSExperimental periodontitis was produced by silk thread sutures combined with high content sugar diet. For HBO therapy, they were exposed to a pressure of 0.25 MPa (2.5ATA), breathing pure oxygen one session a day for 60 min. The treatment course was 2 weeks. The value of PGE(2) in gingiva and alveolar bone was analyzed by enzyme immunoassay (EIA).

RESULTSThe value of PGE(2) in gingiva of control group was 3.21 ng/g, and that of PGE(2) in alveolar bone was 3.22 ng/g. The contents of PGE(2) in gingiva (13.96 ng/g) and alveolar bone (13.32 ng/g) of periodontitis group increased markedly than control group (P < 0.01). The contents of PGE(2) in gingiva (5.21 ng/g) of HBO group were 62.7% which was lower than that of periodontitis group, and the value of PGE(2) in alveolar bone (4.05 ng/g) were 69.6% lower than that of periodontitis group. The difference of PGE(2) in gingiva or alveolar bone was significant for the HBO group and periodontitis group (P < 0.01).

CONCLUSIONSThe contents of PGE(2) in alveolar bone and gingiva increased markedly when experimental periodontitis has formed. The value of PGE(2) in alveolar bone and gingiva reduce markedly after HBO exposure, and the decreased rate of PGE(2) in alveolar bone is more evident than that of PGE(2) in gingiva after HBO therapy.

Alveolar Process ; metabolism ; Animals ; Dinoprostone ; metabolism ; Disease Models, Animal ; Female ; Gingiva ; metabolism ; Guinea Pigs ; Hyperbaric Oxygenation ; Male ; Periodontitis ; metabolism

OBJECTIVE: To detect the concentrations of interleukin-18 (IL-18) and prostaglandin E2(PGE2) in synovial fluid (SF), and to determine the role of IL-18 and PGE2 in osteoarthritis (OA) pathogenesis. METHODS: IL-18 and PGE2 were measured concurrently in synovial fluid samples from 54 patients with knee OA (OA group) and from 9 controls (control group). Quantitative determination of IL-18 was performed by enzyme-linked immunosorbent assay (ELISA). PGE2 was examined by inhibitory enzyme-linked immunosorbent assay. A linear regression between IL-18 and PGE2 was analysed. RESULTS: The concentrations of IL-18 and PGE2 in SF from the OA group were significantly higher than those from the control group (P<0.01). The average value of IL-18 in the control group was (28.768+/-13.575) x 10(-9)ng/L, and (72.303+/-40.130) x 10(-9)ng/L in the OA group (P<0.01); the average value of PGE2 in the control group was (24.697+/-7.814) x 10(-9)ng/L, and (42.302+/-23.818) x 10(-9)ng/L in the OA group (P<0.01). IL-18 was related with PGE2 in a linear curve fashion (the control group: r=0.76, P<0.001; the OA group: r=0.94, P<0.001). CONCLUSION IL-18 and PGE2 are significantly higher in the OA group than those in the control group, and they might take part in the cartilage degradation in OA pathogenesis. The increase of IL-18 might induce the increase of PGE2, and that might play an important role in OA pathogenesis.
Adult ; Aged ; Case-Control Studies ; Dinoprostone ; metabolism ; Female ; Humans ; Interleukin-18 ; metabolism ; Male ; Middle Aged ; Osteoarthritis ; metabolism ; Synovial Fluid ; metabolism