Inhibition of the human placental NAD- and NADP-linked 15-hydroxyprostaglandin dehydrogenases by nonsteroidal anti-inflammatory drugs

Jarabak, Joseph

doi:10.1016/0090-6980(88)90131-1

Cited by 8 publications

(4 citation statements)

References 24 publications

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“…The low plasma concentrations of eicosanoids are a consequence of a combination of instability, as in the case of TxA2 (ti = 30 s at 37°C; [81]), and/or active catabolism, as in the cases of PGE2, PGF2j, PGD2, PGI2 [112][113][114], and leukotrienes [101,112,115,116]. Prostanoid catabolism begins with oxidation of the 15hydroxyl group to yield in one step the 1 5-oxo-derivatives which have 10to 100-fold less activity than the parent compounds.…”

Section: Mechanisms Of Eicosanoid Actionsmentioning

confidence: 99%

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The eicosanoids and their biochemical mechanisms of action

Smith

1989

Biochemical Journal

826

419

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Section: Mechanisms Of Eicosanoid Actionsmentioning

confidence: 99%

“…There are different 1 5-hydroxyprostaglandin dehydrogenases specific for different prostanoids. These dehydrogenases are concentrated in the lung, kidney, and placenta [112][113][114]. The major urinary metabolites of prostanoids are C16 dicarboxylic acids (i.e.…”

Section: Mechanisms Of Eicosanoid Actionsmentioning

confidence: 99%

The eicosanoids and their biochemical mechanisms of action

Smith

1989

Biochemical Journal

826

419

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“…This suggests that panaxynol might not affect the binding of the substrates to the enzyme. Previous studies on bovine lung PGDH (Hansen 1974) and placental PGDH from man (Jarabak 1988) have shown that indomethacin is also a noncompetitive inhibitor for PGDH with regard to NAD+ and PGEl.…”

Section: Discussionmentioning

confidence: 96%

Inhibition of 15-Hydroxyprostaglandin Dehydrogenase Activity in Rabbit Gastric Antral Mucosa by Panaxynol Isolated from Oriental Medicines

Fujimoto¹,

Sakuma²,

Komatsu³

et al. 1998

Journal of Pharmacy and Pharmacology

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Panaxynol is a polyacetylene compound with anti-inflammatory and anti-platelet-aggregatory effects isolated from commonly used oriental medicines. The effects of panaxynol on the activity of prostaglandin-synthesizing and catabolizing enzymes in the rabbit gastric antral mucosa have been examined. At concentrations ranging from 25 to 200 microM panaxynol had no effect on the synthesis of prostaglandins E2, F2alpha and D2 from exogenous arachidonic acid in the microsomal fraction of the gastric mucosa whereas at 25-200 microM it dose-dependently inhibited the activity of 15-hydroxyprostaglandin dehydrogenase (PGDH), which catalyses the initial step of prostaglandin catabolism, in the cytosolic fraction. The concentration required for 50% inhibition (IC50) was approximately 25 microM. Inhibition of PGDH by panaxynol was non-competitive with regard to NAD+ and prostaglandin E2. These results suggest that panaxynol has the potential to inhibit PGDH activity in gastric mucosa, possibly as a result of pharmacological activity.

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“…fetal lung [3], constrict the fetal ductus arter iosus [4,5], inhibit mitotic activity of the skel eton [6], suppress renal maturation [7], and disturb fetal glycogen metabolism [8]. It also alters placental perfusion pressure [9,10], in ducing its degeneration [11], However, it has not been clarified whether corticosteroids ex ert any effect on fetal cardiovascular develop ment during the second trimester. For this reason, we studied the cardiovascular effects of the corticosteroid during the second tri mester of rats.…”

Section: Introductionmentioning

confidence: 99%

Cardiovascular and Pulmonary Effects of Betamethasone during Midtrimester on Fetal Rats

Wu¹,

Momma²,

Akiyama³

1993

Fetal Diagn Ther

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In order to elucidate the effects of corticosteroids on fetal hearts during midtrimester, pregnant rats were injected with a daily dose of betamethasone (1 mg/kg) from the 12th day through the 17th day of pregnancy. The fetal cardiovascular and pulmonary systems were studied on the 21 st day of pregnancy (term). The treated fetuses showed the following signs of hydrops fetalis: retarded growth, pale, edematous skin, and decreased movement. The thymus and lung displayed prominent hypoplasia. The morphometry of the treated fetuses revealed: decreased right ventricle mass by 37% and decreased left ventricle mass by 29 %. We concluded betamethasone had a significant effect on the developing fetal cardiovascular system, inducing hydrops fetalis. Additionally, betamethasone caused hypoplasia of the thymus and lung

show abstract

Inhibition of the human placental NAD- and NADP-linked 15-hydroxyprostaglandin dehydrogenases by nonsteroidal anti-inflammatory drugs

Cited by 8 publications

References 24 publications

The eicosanoids and their biochemical mechanisms of action

The eicosanoids and their biochemical mechanisms of action

Inhibition of 15-Hydroxyprostaglandin Dehydrogenase Activity in Rabbit Gastric Antral Mucosa by Panaxynol Isolated from Oriental Medicines

Cardiovascular and Pulmonary Effects of Betamethasone during Midtrimester on Fetal Rats

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