Concentrations of Prostaglandin A-, E- and F-Like Substances in Gastric Mucosa of Normal Subjects and of Patients with Various Gastric Diseases

Schlegel, Werner; Wenk, Kurt S.; Dollinger, Hans C.; Raptis, Sotirios A.

doi:10.1042/cs0520255

Cited by 29 publications

(13 citation statements)

References 16 publications

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“…This decrease in PGE level may be caused by the cytotoxic effect of the acetic acid injection. However, on the other Days, the PGE levels in non healed rats were higher than those in normal rats, and this finding is in accord with the report by Schlegel et al that the PGE levels were higher in gastric ulcer patients than in normal persons (7).…”

Section: Prostaglandinsupporting

confidence: 80%

Healing process of acetic acid-induced gastric ulcer and gastric mucosal prostaglandin E generation level in rats.

Uchida¹,

Kawano²,

Misaki³

et al. 1989

Jpn.J.Pharmacol

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Abstract-The prostaglandin E (PGE) generation level (PGE level) in the gastric mucosa was investigated in relation to the healing and relapse of acetic acid-induced gastric ulcers in the rat. The PGE level around ulcers showed higher levels after ulcer induction and decreased during the ulcer diminishing period. Thereafter, the PGE levels showed an inclination to increase during the ulcer exacerbation period. In reulcerated rats, PGE levels were significantly higher. In conclusion, a high level of PGE may indicate an ulcer exacerbation state.Prostaglandin has been widely accepted to play an important role in gastric protection. Recently, the present authors reported a correlation between the PG12 level around ulcers and the healing or exacerbation of acetic acid ulcers (1).This communication describes the healing process of acetic acid-induced gastric ulcers observed with an endoscope for 203 days and the results of examining the correlation between the gastric mucosal PGE generation levels (PGE levels) around ulcers and the healing process of acetic acid-induced gastric ulcers.The animals used were Sprague-Dawley strain (Slc:SD) male rats weighing from 220 to 240 g (7 weeks). Acetic acid-induced ulcers were prepared according to the method of Takagi et al. (2) (20%, 0.05 ml). The observation of ulcers and the determination of ulcer-size [Ulcer index (Ul)=length (mm) x width (mm)] were performed according to the method of Fukawa et al. (3) at 3, 10, 20, 35, 50, 70, 91, 112, 133, 154, 175 The UI value was 45.6 on Day 3, and it decreased with time. The first healed case appeared on Day 20 and cumulative healing rate was 46.7% on Day 203. The first relapsed case appeared on Day 50, and the cumulative relapse rate was 46.7% on Day 203. The evolutionary phase of acetic acid-induced gastric ulcers was divided into the following periods as reported previously (6): 1) Ulcer diminishing period (Days 3 to 50 after ulcer induction), 2) healing period (Days 35 to 150 after ulcer induction), and 3) ulcer exacerbation period (Days 50 to 203 after ulcer induction).The time course of the PGE level is shown in Fig. 1. In the present study, on Day 3, the PGE level in the ulcer-induced rats was lower

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Section: Prostaglandinsupporting

confidence: 80%

Healing process of acetic acid-induced gastric ulcer and gastric mucosal prostaglandin E generation level in rats.

Uchida¹,

Kawano²,

Misaki³

et al. 1989

Jpn.J.Pharmacol

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“…A serious side-effect of prolonged indomethacin administration is peptic ulceration. Increasing evidence suggests that in fact this also may be the result of prostaglandin synthesis inhibi tion [33]. In our group of 15 patients who received indomethacin during 1-3 years, a peptic ulcer was seen twice (patients 3 and 17).…”

Section: Discussionmentioning

confidence: 80%

Treatment of the Nephrotic Syndrome with Indomethacin

Donker¹,

Brentjens²,

Hem³

et al. 1978

Nephron

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In 25 patients with nephrotic syndromes of different origin, indomethacin caused an immediate decrease in glomerular filtration rate (GFR) and urinary protein excretion. This effect of indomethacin on GFR and proteinuria was more pronounced when the renin-angiotensin system was stimulated by a low-sodium diet and 50 mg hydrochlorothiazide daily, and resulted in a significant rise in serum albumin. Withdrawal of indomethacin after 1–3 years of administration was followed by an increase in proteinuria to pretreatment levels in 9 out of 15 patients. A harmful renal effect of long-term indomethacin administration was found to be unlikely. The results suggest that the steroid-resistant nephrotic syndrome can be treated symptomatically by indomethacin.

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“…The extracts were redissolved and chromatographed on silicic acid columns as described in [23]. The PGF2, fractions were analyzed with a specific radioimmunoassay [24].…”

Section: Purification Proceduresmentioning

confidence: 99%

Prostaglandin‐E₂ 9‐ketoreductase from human uterine decidua vera

Krùer

Schlegel

1986

European Journal of Biochemistry

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Prostaglandin-E2 9-ketoreductase, the enzyme which catalyzes the reaction from prostaglandin E2 (PGE2) to prostaglandin F2, (PGF2,), has been purified 232-fold from human uterine decidua Vera.The molecular mass of the enzyme, as estimated by fast protein liquid chromatography, was 29 kDa. Sodium dodecyl sulfate disc gel electrophoresis of the denatured enzyme revealed a molecular mass of 31 kDa. These data suggest that the enzyme consists of a single polypeptide chain.The rate equation of the enzyme reaction for two substrates was used for the determination of five kinetic constants. The equilibrium constant with respect to PGE2 was 83 pM, the Michaelis constant, K,, for PGE2 was 93 pM. For NADPH, the equilibrium constant was 1.0 pM and K , was 1.6 pM. The maximal velocity for the forward reaction was V1 = 217 pmol/min. The inhibition constants for the analgesic agents indomethacin and fentiazac were Ki = 850 pM and Ki = 450 pM and for the steroid progesterone Ki = 1.5 mM, respectively.Prostaglandin-E2 9-ketoreductase might be responsible for the control of the PGE2/PGF2, ratio in human decidua Vera. The enzyme, therefore, might be an important factor in the cascade of events leading to uterine contractions and parturition.

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Concentrations of Prostaglandin A-, E- and F-Like Substances in Gastric Mucosa of Normal Subjects and of Patients with Various Gastric Diseases

Cited by 29 publications

References 16 publications

Healing process of acetic acid-induced gastric ulcer and gastric mucosal prostaglandin E generation level in rats.

Healing process of acetic acid-induced gastric ulcer and gastric mucosal prostaglandin E generation level in rats.

Treatment of the Nephrotic Syndrome with Indomethacin

Prostaglandin‐E₂ 9‐ketoreductase from human uterine decidua vera

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Concentrations of Prostaglandin A-, E- and F-Like Substances in Gastric Mucosa of Normal Subjects and of Patients with Various Gastric Diseases

Cited by 29 publications

References 16 publications

Healing process of acetic acid-induced gastric ulcer and gastric mucosal prostaglandin E generation level in rats.

Healing process of acetic acid-induced gastric ulcer and gastric mucosal prostaglandin E generation level in rats.

Treatment of the Nephrotic Syndrome with Indomethacin

Prostaglandin‐E2 9‐ketoreductase from human uterine decidua vera

Contact Info

Product

Resources

About

Prostaglandin‐E₂ 9‐ketoreductase from human uterine decidua vera