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Tuesday, 17 December 2013

The Effects of Hormone Prostaglandins(2)

Prostaglandins, are a group of lipid mediators, found and isolated from human semen in the 1930s by Ulf von Euler of Sweden, responsible for inflammation features, such as swelling, pain, stiffness, redness and warmth. The hormones are produced by almost all nucleated cells and synthesized in the cell from the essential fatty acids (EFAs), include prostacyclin I2 (PGI2), prostaglandin E2 (PGE2), and prostaglandin F (PGF).
11. Prostaglandins and the kidney
In the review of a summary and assessment of research involving renal prostaglandins (Arachidonic acid released from phospholipids is converted by prostaglandin cyclo-oxygenase in the kidney to PGF2, PGF2alpha, PGD2, and, possibly, to PGI2 and thromboxane A2. Production of PGE2 and PGF2alpha is predominately but not exclusively in the medulla, whereas degradative enzymes are present in both cortex and medulla. Prostaglandins enter the tubular lumen by facilitated transport and are partially reabsorbed from the urine in the distal nephron. Urine prostaglandins probably reflect renal synthesis. PGE2 and endoperoxides stimulate and PGF2alpha and indomethacin inhibit renal renin synthesis. In response to ischemia, vasoconstriction, or angiotensin II the kidney increases prostaglandin synthesis to modulate renal vascular resistance), found that in conscious animals or man no role has been established for prostaglandins in the maintenance of basal renal blood flow or renal sodium excretion. PGE influences renal water excretion by inhibiting the action vasopressin. Despite conflicting data there is evidence that renal prostaglandins are involved either primarily or secondarily in many types of hypertension. Inhibitors of prostaglandin cyclooxygenase have been used with success in Bartter's syndrome. Conflicting results in many areas of investigation may be resolved by the use of more accurate and reliable assays, careful handling of samples, and the use of urine to further investigate renal prostaglandin synthesis(11).

12. Prostaglandins in regulating the contraction and relaxation of smooth muscle tissue
According to the Nelson, Randy F. (2005). "An introduction to behavioral endocrinology (3rd ed.). Sunderland, Mass: Sinauer Associates", hormone prostaglandins play an important role in numbers of  physiological effects, including the function of regulating the contraction and relaxation of smooth muscle tissue, by ligating a sub-family of cell surface seven-transmembrane receptors, G-protein-coupled receptors.

13. Prostaglandins and platelet aggregation
Prostaglandins which are derivatives of arachidonic acid including prostaglandin, endoperoxides, thromboxane A2, prostaglandin E2, prostaglandin D2 and prostacyclin. may induce or inhibit platelet aggregation and constrict ro dilate blood vessels. According to the study by Dr. Smith JB.,  it exacerbates ischaemic damage because of a selective increase in vascular resistance due to coronary vasospasm and platelet aggregation which acts to decrease myocardial blood flow. The stable prostaglandins PGD2 and PGE2 are also of interest as both are formed during platelet aggregation. Like PGI2, PGD2 inhibits platelet aggregation(13).

14. Prostaglandin I2 (PGI2) and disaggregation of platelets
In the study to examine the synergistic platelet disaggregating effects among the products of endothelial cells using urokinase, prostaglandin I2 (PGI2), and sodium nitroprusside (SNP) (which is the chemical substitute as nitric oxide(NO)-donor) for endothelium-derived relaxing factor (EDRF), showed that platelet disaggregation rate was increased in a dose-dependent manner and decreased in a time-dependent manner, and the combined use of two or three agents had synergistic effects on platelet disaggregation. Furthermore, flow cytometric analysis showed decreases in the binding of fibrinogen to activated platelets by the addition of PGI2 or SNP. . In addition our data revealed that PGI2 and SNP can act synergistically with fibrinolytic agents. These findings suggest a potential strategy for improving the efficacy of thrombolytic therapy by a combination of these products or their substitutes(14).

15. Platelet prostaglandin H synthase-1 (PGHS-1) deficiency and Bleeding disorder
Defective platelet prostaglandin H synthase (PGHS) activity has been recognized as a cause of bleeding disorders. In the study of a tatal of three female patients aged 37, 48 and 55 who presented with a mild bleeding disorder due to platelet dysfunction, showed that human platelet PGHS-1 deficiency is due to two types of enzyme defects: type 1 defect is manifested by an undetectable PGHS-1 protein in platelets whereas the type 2 defect is manifested by a normal quantity of PGHS-1 protein which has an impaired catalytic activity(15).

16. Prostaglandins E2 and labor
In the study to determine safety of induction of labor with vaginal Prostaglandins (E2) in Grand Multipara., showed that in a total of 50% cases were induced for past dates, the ceasarean rate was high in the induction group (19.5%) compared to the control (12.5%) OR 1.69 RR 1.37(95% CI-1.07-1.75) difference was statistically significant. Adverse neonatal outcome was found to be similar in both groups. Special Care Baby Unit (SCBU) admissions were 19 in the induction group and 21 in the control group, which was not statistically significant. No severe maternal complications were observed such as infection or uterine rupture(16).

17. Hormone Prostaglandins sensitize spinal neurons to pain
A number of prostaglandins (PGs) sensitize dorsal root ganglion (DRG) neurons and contribute to inflammatory hyperalgesia by signaling through specific G protein-coupled receptors (GPCRs). According to the study by the Washington University Pain Center, suggested that 15d-PGJ2 induces activation followed by persistent inhibition of TRPA1 channels in DRG sensory neurons in vitro and in vivo. Moreover, we demonstrate novel evidence that 15d-PGJ2 is analgesic in mouse models of pain via a TRPA1-dependent mechanism. Collectively, our studies support that TRPA1 agonists may be useful as pain therapeutics(17).

18. Hormone Prostaglandins and Intraocular pressure (IOP)
Intraocular pressure (IOP) reduction is currently the only therapeutic approach demonstrated to preserve visual function in patients with glaucoma. According to the study by Universit Joseph Fourier (UJF), Grenoble, in the study to review of published studies evaluating the efficacy and tolerability of the IOP-lowering unfixed and fixed combination therapies with PGAs, indicated that
α(2)-adrenergic agonists-PGA and carbonic anhydrase inhibitor-PGA combinations seem to be at least as effective at reducing IOP as the β-blocker-PGA combinations. As for the fixed combinations, the review shows that the three PGA-timolol fixed combinations are more effective than their component medications used separately as monotherapy and are better tolerated than the three respective prostaglandins(18).

19. prostaglandins and inflammatory mediation
Overproduction of prostaglandins has been considered in mediation of inflammation and carcinogenic process. In the study to search  for anti-inflammatory and chemopreventive agents from natural products, bioassay-guided fractionation led to the isolation of curdione from the rhizome of Curcuma zedoaria with the inhibitory effect on the production of prostaglandin E2 in lipopolysaccharide (LPS)-stimulated mouse macrophage RAW 264.7 cells in a concentration-dependent manner (IC50 = 1.1 microM). Mechanistic studies suggest that the suppression of cyclooxygenase-2 (COX-2) mRNA expression is, at least in part, involved in this inhibitory activity of curdione, according to the study by the Ewha Womans University, Seoul.(19).

20. Prostaglandin E2 and tooth movement
In the study to to investigate the occurrence of orthodontic root resorption in connection with local injection of prostaglandin E2 (PGE2) consisting 25 male Wistar rats, in the duration of experiments was 3 days, 7 days, and 10 days, showed that the maxillary first molars on both sides were each moved mesially by means of a coil spring. On the right side 0.1 ml of PGE2 0.1 micrograms/microliters was injected in the gingiva on the buccal side of the upper first molar on days 0, 3, 5, and 7. On the left side no injection of PGE2 was performed. In three animals in the 7-day group the vehicle (Waymouth medium) was injected. There was no significant difference in root resorption between the experimentally moved teeth with and without local injection of PGE2, but a trend towards more root resorption was registered on the teeth where such injections had been performed(20).
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