Effect Of Prostaglandin A1 Research Articles

Effect of prostaglandin A1 in porcine cells persistently infected with classical swine fever virus.

Cyclopentenone prostaglandins are potent inhibitors of a wide variety of RNA and DNA viruses. In this report we describe that prostaglandin A1 (PGA1) potently inhibited the replication of classical swine fever virus in cultures of PK-15 cells. The highest non-toxic dose (5 microg/ml) inhibited virus yield in 99% at the initial phase of infection and in 77% in persistent infected cells. However when PGA1 was removed from persistently infected cells, the inhibition of virus replication was partially reverted.

Inhibition of rotavirus replication by prostaglandin A: evidence for a block of virus maturation.

Rotaviruses are recognized as the leading cause of severe viral gastroenteritis in young children and in immunocompromised patients. Cyclopentenone prostaglandins possess antiviral activity against several single-strand RNA viruses; therefore, the effect of prostaglandin A1 (PGA1) on SA-11 simian rotavirus infection was investigated in cultured cells. PGA1 potently inhibited SA-11 rotavirus replication. Whereas it did not affect virus adsorption or penetration, PGA1 partially inhibited VP4 and VP7 synthesis and selectively reduced glucosamine incorporation into the NSP4 viral enterotoxin. Electron microscopy analysis showed that, despite normal formation of cytoplasmic inclusions and budding of particles into the rough endoplasmic reticulum, virus maturation was impaired in PGA1-treated cells, with most of the virus particles remaining in the membrane-enveloped intermediate form. Because prostaglandins are used clinically as cytoprotective drugs for gastric ulcers, these observations offer new perspectives in the search for therapeutic agents for rotavirus-induced gastroenteritis.

Effect of prostaglandin A1 in the induction of stress proteins in Aedes albopictus cells.

Prostaglandins are natural fatty acid derivatives with diverse physiological effects, including immune function and the control of cell growth. While the action of prostaglandins in the induction of stress proteins in vertebrate cells is well documented, their functions in invertebrate cells have been poorly investigated. The purpose of the present study was to investigate the effect of prostaglandin A1 (PGA1; 0.25, 1.25 and 12.5 micrograms/ml) on protein synthesis during the growth of Aedes albopictus cells. We found that PGA1 stimulates the synthesis of several polypeptides with molecular masses of 87, 80, 70, 57, 29, 27 and 23 kDa in Aedes albopictus cells. When the proteins induced by PGA1 and those induced by heat treatment were compared by polyacrylamide gel electrophoresis, PGA1 was found to induce the stress proteins. The HSP70 family and the low-molecular weight polypeptides (29 and 27 kDa, respectively) were induced by PGA1 in the lag phase. We also observed that PGA1 is able to induce a 23-kDa polypeptide independently of the growth phase of the cell.

Effect of prostaglandin A1 on renal hemodynamics in pregnancy toxemia

PGA1 was infused at a constant rate for 2 hours in 35 pregnant women in the third trimester. Twenty-five patients had clinical manifestations of pregnancy toxemia and 10 served as control subjects. Two dose levels (0.5 to 1.0 mug/kg/min) were investigated and obstetric aspects as well as renal hemodynamics were evaluated. At the high-dose level, the drug induced labor in half the subjects (toxemia patients and control subjects) and elicited a hypotensive response only in hypertensive cases. A marked increase in GFR and RPF was achieved at both dose levels in all cases. Plasma electrolytes, osmolality, and urea levels were unaltered. Also, the infusions did not induce any appreciable diuresis or natriuresis. Tph mechanisms of the induced changes and possible etiologic involvement of PGA1 in toxemia are discussed.

The effect of prostaglandin A1 on renin and aldosterone in man.

Blood pressure, pulse rate, plasma aldosterone (PA), renin, and cortisol were monitored during graded intravenous infusions of prostaglandin At (PGA)1), 0.075-0.6 mug/kg min-1, alone and superimposed on angiotensin II (A II) administration in five normal men. The infusions of PGA1 did not affect blood pressure, but did progressively increase the pulse rate up to 15.2 +/- 2.0 (SEM- beats/min at the highest prostaglandin dose (0.6 mug/kg min-1). Both PA and plasma renin activity (PRA) increased in a dose-related fashion in response to the prostaglandin infusions. Aldosterone increased from a control of 4.8 +/- 0.4 to 20.7 +/- 1.2 ng and PRA increased from 0.9 +/- 0.1 to 5.4 +/- 0.4 ng/ml hr-1 at the dose of 0.6 mug/kg min-1. The correlation between the aldosterone and renin values was r = 0.85 P less than 0.001. In separate experiments, acute volume expansion with 2 liters of saline did not affect the increase in renin activity induced by exogenous prostaglandin. A II (5 ng/kg min-1) increased aldosterone and blood pressure and decreased the pulse rate. The hemodynamic effects were progressively reversed by the superimposed prostaglandin infusions, but the observed changes in renin and aldosterone concentrations were not further altered. The PA response to A II infusions was not influenced by indomethacin pretreatment. Prostaglandin A (infusion) appears to have a direct effect on renin release in man.

Inhibition of Gastric Secretion in Man by Prostaglandin A1

The effect of prostaglandin A1 (PGA1) on gastric secretion was evaluated in 18 healthy volunteers. PGA1 was infused for 30 min in low dose (0.5 to 0.6 μg per kg per min) to 9 subjects and in a higher dose (1.0 to 1.25 μg per kg per min) to 9 subjects, after a steady state of submaximal gastric output was obtained by administration of intravenous histamine (0.015 mg per kg per hr). PGA1 significantly inhibited mean volume and acid output, respectively, by 30% and 25% during PGA1 infusion. Following discontinuance of infusion of PGA1, mean volume and acid output were, respectively, 98% and 103% of control levels. PGA1 was well tolerated by all subjects. There was no correlation between the gastric secretory response to PGA1 infusion and plasma glucose, cortisol, immunoreactive insulin, or growth hormone levels or arterial blood pressure. Plasma free fatty acid levels and pulse rate were significantly increased during PGA1 infusion.