Prostaglandins
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 F2α (PGF2α).
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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Sources
(11) http://www.ncbi.nlm.nih.gov/pubmed/333946
(13) http://www.ncbi.nlm.nih.gov/pubmed/7034481
(14) http://www.ncbi.nlm.nih.gov/pubmed/10839560
(15) http://www.ncbi.nlm.nih.gov/pubmed/8562397
(16) http://www.ncbi.nlm.nih.gov/pubmed/22224182
(17) http://www.ncbi.nlm.nih.gov/pubmed/23013719
(18) http://www.ncbi.nlm.nih.gov/pubmed/22686588
(19) http://www.ncbi.nlm.nih.gov/pubmed/18038902
(20) http://www.ncbi.nlm.nih.gov/pubmed/1717297
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