Biomedical subjects
Publications and source records attributed to S Ota.
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The effect of cAMP on prostaglandin production may depend on cell types. To clarify the relationship between PG and cAMP, we examined arachidonate's effects on PG synthesis and intracellular cAMP accumulation in monolayers of rat gastric mucosal cells. These cells produced PGE2, PGI2 and thromboxaneA2 (TXA2) in amounts of 316 +/- 18, 100 +/- 7 and 30 +/- 5 pg per 10(5) cells in 10 min, respectively, in response to 10 microM arachidonic acid (AA). The production of these PG, however, leveled off subsequently. Cells initially exposed to AA responded poorly to a subsequent stimulation by AA. AA simultaneously stimulated intracellular cAMP accumulation; this stimulatory effect on cAMP production was abolished by the pretreatment with indomethacin. Nevertheless, the pretreatments with dibutyryl cAMP (0.1-5 mM) did not alter the amount of subsequent AA-induced PGE2 production. Furthermore, the preincubation with 1mM isobutyl methyl xanthine also failed to affect PGE2 synthesis, while it increased intracellular cAMP accumulation. Our studies suggest AA stimulates intracellular cAMP formation in cultured gastric mucosal cells, linked with conversion of AA to cyclooxygenase metabolites, AA-induced PG production is limited in these cells, and it seems, however, unlikely that intracellular cAMP modulates AA metabolism to PG.
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Aim of this study was to investigate the effect of geranylgeranylacetone (GGA) on mucus synthesis and secretion in rat gastric cultured cells, and their relationship to prostaglandin (PG) synthesis. Rate of mucus synthesis was estimated by incorporation of 3H-glucosamine into the cultured cells. Release of 3H-glucosamine from the cells, which were preincubated in the medium containing the radioactive isotope, into the culture media was measured for the evaluation of mucus secretion. PG production by the cultured cells was measured by radioimmunoassay. GGA increased glycoprotein synthesis in a dose-dependent manner (p less than 0.01). Secretion of mucus from cultured cells was also significantly enhanced by GGA. GGA did not significantly increase PG (E2 and I2) production. These results indicate that GGA has the ability to stimulate mucus production by the gastric epithelial cells, and this action may play an important role in protective effect of GGA. It is, however, unlikely that this effect of GGA is mediated by endogenous PGs.
The purpose of this study was to investigate the morphological and physiological effects of tetraprenylacetone (TPA) on ethanol(ET)-induced injury in rat gastric mucosa. Fasted rats received orally the following agents; a) vehicle (VH); b) 50, 100, or 200 mg/kg of TPA; c) indomethacin (IDM, 5 mg/kg), 30 min prior to TPA (200 mg/kg). Thirty minutes later, 1 ml of absolute ET was administered into the rat stomach. The gastric mucosa was assessed at 60 min after administration of ET. The ulcer index was significantly decreased by TPA in a dose-related fashion when compared with controls. Histological studies also showed significant reduction of ET-induced mucosal damage by TPA. A scanning electron microscopic study revealed that, when TPA was administered, surface epithelial cells of fundic mucosa were protected against ET-induced injury. The decrease of potential difference induced by ET was diminished by TPA (p less than 0.01). Addition of IDM significantly reduced the effect of TPA. This indicates that TPA has a protective effect on rat gastric mucosa against ET-induced injury. The data also suggested that endogenous prostaglandins may be partially involved in this effect of TPA.
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Whether cimetidine protects gastric mucosal cells independently of its antisecretory effect has been controversial. Some investigators postulate that, on the contrary, cimetidine decreases the integrity of gastric mucosa. Furthermore, whether cimetidine influences gastric prostaglandin (PG) synthesis is debated. Therefore, we investigated and compared with 16,16-dimethyl-PGE2 (dmPGE2) whether cimetidine protects cultured rat gastric mucosal cells from indomethacin, and tested whether cimetidine affects gastric PG production by these cells. Cell damage was assessed by chromium 51-release assay. Concentrations of indomethacin greater than 1 mmol/L caused cell damage and increased 51Cr release in a dose-dependent and time-dependent fashion. dmPGE2 significantly reduced indomethacin-induced increase of 51Cr release, whereas cimetidine at both nonantisecretory and antisecretory doses did not alter 51Cr release caused by indomethacin. The cultured cells released PGE2 and PGI2 in amounts of 215 +/-18 and 56 +/- 3 (mean +/- SEM) pg/10(5) cells in 1 hour, respectively. Nondamaging concentrations of indomethacin caused a dose-dependent inhibition of PG release from cultured cells with 50% inhibitory concentration at a dose of 10(-6) to 10(-7) mol/L. Cimetidine did not alter gastric PG production. In summary, exogenous PG protected gastric mucosal cells from indomethacin in vitro, but cimetidine did not. In conclusion, cimetidine, which fails to affect gastric PG production, does not directly influence the integrity of gastric mucosal cells.
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To check whether crude stem and fruit bromelains can be fractionated further or not, systematic separation procedures were applied to both enzymes. Six proteolytically active components, which were designated as SBB 1-5 and SBA, were fractionated from crude stem bromelain by successive use of gel filtration on Sephadex G-75, and chromatographies on CM-Sephadex and DEAE-Sephacel. One main and one minor active components, designated as FBA and FBB, respectively, were also separated from crude fruit bromelain by chromatographies on DEAE-Sephacel and then CM-Sephadex. Some of the physico-chemical and enzymatic properties of these eight components were compared. Each component migrated as a single band on SDS-polyacrylamide gel electrophoresis. Molecular weights determined by the same electrophoresis were about 27,000 for SBB 1-3 and FBB, and about 23,000 for the other four components. In terms of amino acid composition, FBB resembled SBB 1-3, which were remarkably similar to each other. FBA was also similar to SBA in amino acid composition, and contained much less basic amino acids than SBB 1 through 5. The principal amino-terminal residues determined by the cyanate method were valine in SBB 1-5 and SBA, and alanine in FBA and FBB. The principal carboxyl-terminal residues determined by the hydrazinolysis method were glycine in SBB 1-3, SBA and FBA, and serine in SBB 4-5 and FBB. However, fractional amounts of a few other amino- and carboxyl-terminal residues were also detected. As regards enzymatic activities, FBA and SBB 4 and 5 were much more active than the other five components against casein and some synthetic substrates [Bz-Arg-amide (at pH 6.1), Z-Gly-X, and Z-Ala-X (at pH 3.5)] with the notable exception that FBA was much less active than SBB 4 and 5 toward tripeptides (X-Gly-Gly).
With a quantitative blood endotoxin assay using a chromogenic substrate with a perchloric acid pretreatment (PCA-LCT), endotoxemia in various liver diseases was studied. With PCA-LCT, recovery of added endotoxin in human plasma was nearly 90%, as evidenced by an intra- and inter-assay coefficients of variation of 5.7% and 11%, respectively. Because the recovery of endotoxin was not affected in severely icteric plasmas, PCA-LCT proved to be applicable to patients with liver diseases where various degree of jaundice exist. In none of the plasmas from patients with chronic hepatitis, acute hepatitis without hepatic failure or liver cirrhosis without ascites did the endotoxin level exceed the normal range of less than 5 pg/ml. With the presence of ascites, however, endotoxemia became detectable, but at low levels and not in all cases. At the stage of hepatic failure complicated with renal failure or disseminated intravascular coagulation, endotoxemia was more frequent and endotoxin concentration greater. It is uncertain, at present, whether endotoxemia itself is deteriorating factor in hepatic failure or is merely concomitant phenomenon resulting from Kupffer cell failure.
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