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PubMed2006

Effects of plastoquinones from the brown alga Sargassum micracanthum and a new chromene derivative converted from the plastoquinones on acute gastric lesions in rats.

Previously, we reported the anti oxidative and anti viral effects of plastoquinones (compounds 1, 2) extracted from the seaweed Sargassum micracanthum (Kuetzing) Endlicher and a new chromene compound (compound 3), which was converted from the plastoquinones. Recently, we have also demonstrated the antiulcer effects of these compounds and assessed the effects using a rat model of acute gastric lesion and fundus strips isolated from rats. In hydrochloric acid/ethanol rat ulcer tests: 1) oral administrations of compounds 1, 2, and 3 1--10, 3--30 and 10--30 mg/kg, respectively, and omeprazole 3--30 mg/kg showed dose-dependent antiulcer effects: 2) the antiulcer effects after intraduodenal administration of the respective compounds at the dose of 30 mg/kg were found to be significant: and 3) a decrease in the hexosamine level of the gastric mucosa was slightly improved by oral administration of compounds 1, 2, and 3 30 mg/kg. In indomethacin-induced gastric ulcer tests, the antiulcer effects of compounds 1, 2, and 3 10 mg/kg (p.o.) were not significant. Compounds 1, 2, and 3 showed slight contracting effects on the fundus isolated from rats and these effects were inhibited by pretreatment with AH6809, an inhibitor of prostaglandin DP, EP(1), and EP(2) receptors. These results suggest that the protection of the mucosa via endogenous prostaglandins might be related to the antiulcer effects of compounds 1, 2, and 3.

Acute Disease↗
PubMed2006

Anti-ulcer effect of tea catechin in rats.

Oral administration of tea catechin dose-dependently prevented absolute ethanol-induced (50, 100, 200 mg/kg) or restraint plus water immersion stress-induced acute gastric mucosal injury (300, 400 mg/kg) in rats. When the effect of test compound was evaluated on the 15th day after acetic acid injection to rats, repeated oral administration of tea catechin (25, 50, 100 mg/kg twice daily) dose-dependently accelerated the healing of acetic acid-induced chronic gastric ulcers. Tea catechin (10(-5)-10(-1) g/100 ml) concentration-dependently scavenged superoxide anions in vitro. Tea catechin (100, 200 mg/kg orally) markedly inhibited the increase in thiobarbituric acid-reactive substances in the injured mucosa of rats treated with 50% ethanol. Tea catechin (50, 100 mg/kg twice orally, daily) markedly inhibited the increase in content of thiobarbituric acid-reactive substances in the ulcerated region of acetic acid-induced gastric ulcers on the 7th and 15th days. In addition, at 50, 100 and 200 mg/kg orally, it dose-dependently prevented the decrease in gastric mucosal hexosamine content induced by absolute ethanol, although it failed to inhibit the basal gastric acid secretion. These results suggest that tea catechin may primarily protect gastric mucosa from acute gastric mucosal injury and promote the healing of chronic gastric ulcers by its antioxidant activity and gastric mucus-increasing actions.

Acetic Acid↗
PubMed2006

Effect of oral vitamin E administration on acute gastric mucosal lesion progression in rats treated with compound 48/80, a mast cell degranulator.

The effect of oral vitamin E administration on acute gastric mucosal lesion progression was examined in rats treated once with compound 48/80 (C48/80) (0.75 mg/kg, i.p.) in comparison with that of subcutaneously administered superoxide dismutase (SOD) plus catalase (CAT). Vitamin E (50, 100 or 250 mg/kg) administered at 0.5 h after C48/80 treatment reduced progressive gastric mucosal lesions at 3 h after the treatment dose-dependently, like SOD plus CAT administered at the same time point. The gastric mucosa of C48/80-treated rats had decreased Se-glutathione peroxidase activity and vitamin E, ascorbic acid, and hexosamine contents and increased myeloperoxidase and xanthine oxidase activities and thiobarbituric acid reactive substances content at 3 h after the treatment. Administered vitamin E attenuated all these changes found at 3 h after C48/80 treatment dose-dependently, like administered SOD plus CAT. C48/80-treated rats administered with vitamin E (100 or 250 mg/kg) had higher gastric mucosal vitamin E content than C48/80-untreated rats. Neither administered vitamin E nor SOD plus CAT had any effect on the increases in serum serotonin and histamine concentrations and the decrease in gastric mucosal blood flow found at 3 h after C48/80 treatment. In the gastric mucosa of C48/80-untreated rats administered with vitamin E, thiobarbituric acid reactive substances content decreased with an increase in vitamin E content. These results indicate that orally administered vitamin E prevents acute gastric mucosal lesion progression in C48/80-treated rats possibly by suppressing oxidative stress, neutrophil infiltration, and mucus depletion in the gastric mucosa like administered SOD plus CAT.

Animals↗
PubMed1982

The etiology of caffeine-induced aggravation of gastric lesions in rats exposed to restraint plus water-immersion stress.

Caffeine augmented formation of gastric lesions in rats exposed to restraint plus water-immersion stress for 3 h, together with inhibition of gastric secretion and gastric motility. The etiology of the lesion aggravation by caffeine was studied by measuring several parameters which were relevant to the mucosal defensive factors. Caffeine increased the susceptibility of gastric mucosa to erosive action of acid when simultaneously combined with the stress procedure. Injection of caffeine via an intraperitoneal route, but not via an intraarterial route, caused a decrease in gastric tissue blood flow when no marked fall in body temperature was seen. This indicates that the caffeine-induced decrease in gastric tissue blood flow is not due to its direct action on the gastric mucosal vessels. Hexosamine content of gastric wall tissues, however, was not significantly changed in caffeine-pretreated rats at 3 h after stress. These results suggest that caffeine aggravates stress-induced gastric lesions through some mechanism in reducing mucosal blood flow which is responsible for liability of mucosal autodigestion.

Animals↗
PubMed1991

[Effect of AS-2646, a novel antiulcer agent on gastric mucosal defensive factors in rats].

The effects of AS-2646 on the acute gastric mucosal lesions induced by various noxious agents and the gastric mucosal defensive factors were studied in rats, and the following results were obtained: 1) AS-2646 (5-100 mg/kg, p.o.) dose-dependently inhibited the formation of the mucosal lesions induced by ethanol, ethanol-HCl, taurocholate-HCl and serotonin, and its anti-lesion spectrum was the widest among the compounds (cimetidine, pirenzepine, sulpiride and prostaglandin E1) examined here. 2) AS-2646 (5-10 mg/kg, p.o.) not only improved the changes of gastric mucosal hemodynamics induced by the blood removal and/or the reserpine treatment, but also inhibited the mucosal lesions induced by them. 3) AS-2646 (2-20 mg/kg, p.o.) antagonized the decrease in the surface gastric mucus and mucosal hexosamine contents induced by stress and/or aspirin. 4) AS-2646 (2-20 mg/kg, p.o.) caused no significant effect on the gastric mucosal prostaglandin E2 levels. 5) AS-2646 inhibited Campylobacter pylori in vitro. These results indicate that AS-2646 may be useful as a novel antiulcer drug with the defensive factor-potentiating and anti-Campylobacter pylori effects.

Animals↗
PubMed1978

Pharmacological studies on experimental nephritic rats (3). Changes in the connective tissue components of renal cortex in the modified type of Masugi's nephritis.

Using a modified type of Masugi's nephritis, quantitative changes in several connective tissue components of renal cortex during the process of nephritis were compared with those of the contents of urinary protein and serum cholesterol. Levels of urinary protein and serum cholesterol were highest 10 days after anti-kidney serum injection and nearly normal levels were reverted to on the 30th day. The levels of sialic acid, uronic acid and hydroxyproline in the renal cortex of the nephritic group significantly increased from the 1st, 5th and 10th days, respectively compared with the normal group. The sialic acid content reached a peak with an increase of approx. 40% on the 15th day, reverting to almost the normal level on the 30th day, while the uronic acid and hydroxyproline levels continued to increase slowly after the 15th day, reaching rates of approx. 70% and 40%, respectively on the 30th day. The hexosamine content reached a maximum of 20% on the 20th day. Quantitative changes in connective tissue components of the renal cortex due to nephritis appear to reflect the degree of the repair of injured renal tissue.

Animals↗
PubMed1979

Changes in connective tissue components in ulcer tissue during the healing process of acetic acid ulcer in rats.

In order to elucidate the role of connective tissue components on the repair of ulcerated regions, quantitative changes in chemical components in ulcer tissue during the healing process were investigated in acetic acid-induced ulcer in rats. The ulcer index showed a peak on the 5th day after the operation, declined rapidly and maintained a slight level the 15th to the 60th days, without a complete recovery. In ulcer tissue, sialic acid and hexosamine remarkably increased in the early stages of healing, showing a peak on the 5th day. The patterns of time course of changes in both components ran almost parallel with those in the ulcer index. Uronic acid maintained slightly higher levels than normal levels the 5th to the 60th days. Hydroxyproline continued to increase with the time course from the 25th day. When acid mucopolysaccharides in ulcer tissue were isolated into various fractions, there were increases in hyaluronic acid on the 5th day, in chondroitin sulfate A and chondroitin sulfate C on the 30th day and chondroitin sulfate B on the 60th day, respectively. Significance of changes in these components in the healing process is discussed.

Acetates↗
PubMed1982

Effects of the antiulcer drug geranylgeranylacetone on aspirin-induced gastric ulcers in rats.

Antiulcer effects of geranylgeranylacetone (GGA) on aspirin-induced gastric ulcers in rats were studied, comparing them with those of gefarnate. The oral administration of GGA prevented the development of gastric ulcer induced by a single or repeated oral administration (5 consecutive days) of aspirin. The effects of GGA were more potent and more definite than those of gefarnate. The intraduodenal administration of GGA, but not the intragastric administration, also inhibited the ulceration induced by aspirin in pylorus-ligated rats, while the intraduodenal administration of gefarnate did not. GGA prevented the reduction of the H+ concentration and the increment of Na+ concentration in the gastric juice induced by aspirin. In addition, the decrease of hexosamine content in the gastric mucosa induced by aspirin was restored to a normal level by GGA, but not by gefarnate. From these results, it was concluded that the protective actions of GGA on aspirin-induced gastric ulcers might be due to its protection from the weakening of gastric mucosal resistances.

Animals↗
PubMed1991

Effects of the new anti-ulcer agent KB-5492 on experimental gastric mucosal lesions and gastric mucosal defensive factors, as compared to those of teprenone and cimetidine.

Effects of KB-5492, a new anti-ulcer agent, on various experimental gastric mucosal lesions and mucosal defensive factors in rats were compared with those of teprenone and cimetidine. KB-5492 administered orally at 12.5-200 mg/kg inhibited water-immersion stress- and indomethacin-induced gastric mucosal lesions in a dose-dependent manner with ED50 values of 46 and 27 mg/kg, respectively, indicating that KB-5492 was more potent than teprenone but less potent than cimetidine. KB-5492, administered orally at 12.5-100 mg/kg, also inhibited ethanol-induced gastric mucosal lesions in a dose-dependent manner with an ED50 of 23 mg/kg, so KB-5492 was 3 times more potent than teprenone, whereas cimetidine produced no obvious inhibition. In addition, KB-5492, administered orally at 25 and 50 mg/kg twice daily for 10 consecutive days, significantly accelerated the healing of acetic acid-induced gastric ulcers more potently than teprenone and cimetidine. KB-5492 at anti-ulcer doses significantly increased gastric mucosal blood flow in normal anesthetized rats and inhibited the reduction of gastric mucosal hexosamine content induced by aspirin, but did not affect gastric acid secretion in pylorus-ligated rats. These results indicate that KB-5492 has potent and broad anti-ulcer properties, which are probably exerted by its enhancement of gastric mucosal defensive factors through increasing gastric mucosal blood flow and/or retaining gastric mucus, and not by its inhibition of gastric acid secretion.

Administration, Oral↗
PubMed1994

Effects of NC-1300-O-3 on gastric mucus secretion and prostaglandin release in rats.

We investigated the effect of NC-1300-O-3 on gastric mucus secretion and prostaglandin release into the gastric lumen in rats. NC-1300-O-3 following single or repeated administration for up to 4 weeks significantly increased the hexose content in the gastric lumen at 10 to 100 mg/kg, p.o. Omeprazole and cimetidine at doses that strongly inhibited gastric acid secretion had no effect on the hexose content following single or repeated administration for 8 days. When administered repeatedly for 8 days, NC-1300-O-3, omeprazole and cimetidine significantly decreased the hexosamine content in gastric surface mucosa, but significantly increased gastric mucus secretion was observed at the same time only with NC-1300-O-3, indicating that this agent has a profile of action on gastric mucus metabolism different from those of omeprazole and cimetidine. NC-1300-O-3 at 10 and 30 mg/kg, p.o. and omeprazole at 30 mg/kg, p.o. increased the release of prostaglandins into the gastric lumen, and this was markedly inhibited by pretreatment with indomethacin, suggesting that these agents may enhance prostaglandin biosynthesis in the gastric mucosa. From these results, it seems that the enhancement of NC-1300-O-3 on gastric mucus secretion and prostaglandin biosynthesis in the gastric mucosa contribute to the antiulcer effect of NC-1300-O-3.

Animals↗
PubMed1998

Role of glutathione in the antiulcer effect of hot water extract of black tea (Camellia sinensis).

The role of a hot water extract of black tea (Camellia sinensis (L). O. Kuntze Theaceae) in the gastric cytoprotective mechanisms was studied using gastric mucosal lesions produced by various ulcerogens in rats as an experimental model. Prior oral administration of black tea extract (BTE) at 20 ml/kg, i.g. once a day for 7 days significantly reduced the incidence of gastric erosions and severity induced by ethanol, diethyldithiocarbamate (DDC) and diethylmaleate (DEM). This treatment also favorably altered the changes in acid and peptic activity of gastric juice in these ulcerogen-treated animals. Singular administration of succimer (60 mg/kg, i.g.), the standard sulfhydryl containing antiulcer drug used as a reference drug, was also effective. The levels of glutathione and glutathione peroxidase were significantly decreased after treatment with ethanol, DDC and DEM, and this decrease was prevented by BTE pretreatment in the aforesaid manner. Other major features of BTE-induced reversal of ulcerogenic agents include a significant decrease in the protein content and a marked increase in hexosamine and sialic acid content. These results suggest a major role for glutathione, an endogenous antioxidant, in the cytoprotection against ulceration afforded by BTE.

Animals↗
PubMed1998

Teprenone, an anti-ulcer agent, increases gastric mucosal mucus level via nitric oxide in rats.

We examined whether the increasing action of teprenone (TP) on mucus synthesis and content in rat gastric mucosa is related to nitric oxide (NO) formation via NO synthase (NOS) in the tissue. TP (200 mg/kg)-induced increases in levels of gastric mucosal hexosamine and adherent mucus were inhibited with decreased gastric mucosal NOS activity and nitrite/nitrate concentration by co-administration of NG-monomethyl L-arginine (100 mg/kg), a NOS inhibitor, but not its D-isomer. These results suggest that TP exerts an increasing action on gastric mucus synthesis and content possibly under the condition of maintained NO production via NOS in gastric mucosal tissues, although the precise mechanisms for the action of TP is still unclear.

Animals↗
PubMed2006

The impact of nutrition of the cumulus oocyte complex and embryo on subsequent development in ruminants.

Cumulus-oocyte complexes (COCs) and early embryos rely on a histotrophic nutrition source for energy production and the synthesis of macromolecules. There is accumulating evidence suggesting that the balance of supply and demand for energy and other anabolic substrates during oocyte maturation and very early stages of development programmes subsequent developmental potential, and this may include subsequent fetal growth trajectory. One example is the role of glucose (Glc) during cumulus-oocyte complex maturation. Glucose is an essential nutrient for maturation, especially its role during cumulus expansion. Our laboratory has shown that during in vitro culture, too little glucose during cumulus-oocyte complex maturation affects meiotic competence. We have focussed on glucose (Glc) metabolism through the hexosamine biosynthesis pathway (HBP) during COC maturation in vitro. The HBP in somatic cells is regarded as a "fuel-sensing" pathway and its interaction with cell signalling systems and transcriptional regulation is increasingly apparent. Up-regulation of the HBP during oocyte maturation in vitro has negative consequences for subsequent development. Another example is the role of hypoxia (low O2) during peri-compaction development. My laboratory believes that ruminant embryos during compaction, blastulation and subsequent development in the uterine cavity lack a key hypoxia responsive element. Because of this, hypoxia is important for normal development in ruminants but perturbs further development in rodents. The implication of these examples to the fundamental concept of peri-conception nutritional programming of development are discussed.

Animal Nutritional Physiological Phenomena↗
PubMed1999

New method for determining the sugar composition of glycoproteins, glycolipids, and oligosaccharides by high-performance liquid chromatography.

A new method is reported that can be performed within a single vessel to analyze the composition of aldose, hexosamine, and sialic acid residues of glycoproteins, glycolipids, and oligosaccharides. Glycoconjugates are treated with sialidase or subjected to mild acid hydrolysis, before being treated with N-acetylneuraminic acid aldolase to convert the free sialic acid residues to their corresponding N-acylmannosamines. The reaction mixture is then successively subjected to acid hydrolysis (in order to produce monosaccharides), N-acetylation, and conversion with p-aminobenzoic acid ethyl ester (ABEE). The ABEE-converted monosaccharides are simultaneously determined by reverse-phase high-performance liquid chromatography. Determination of the sugar compositions of bovine fetuin, II3NeuGc alpha-LacCer, and 3'-sialyllactose with this method was found to be highly accurate. Linearity of the peak area vs. the amount of bovine fetuin ranged from 1 to 50 micrograms in all ABEE-converted monosaccharides. With a slight modification to this method, sialic acid residues can be separately determined as NeuAc and NeuGc. This novel method and its modified version are used to demonstrate the sugar compositions of alpha 1-acid glycoproteins from several sources.

Acetylation↗
PubMed2006

Ethanol-induced changes in glycolipids of Saccharomyces cerevisiae.

Total glycolipid content of Saccharomyces cerevisiae cells increased in ethanol-treated yeast cells. Sialic acid and hexosamine contents of glycolipids from ethanol-treated cells decreased, whereas those of hexoses increased. Increased sialidase activity in the presence of ethanol may be responsible for the decrease in sialic acid content of glycolipids. The saccharide moieties of glycolipids of S. cerevisiae consisted of fucose, mannose, galactose, and glucose. Ethanol treatment of yeast cells caused an increase in glucose and a decrease in galactose content of glycolipids. The changes in glucose content can be related to changes in beta-glucosidase activity under alcohol stress. The content of cerebrosides, sulfatides, and monoglucosyldiglycerides was enhanced following ethanol treatment. An increase in cerebroside as well as in sulfatide content during alcohol stress might play an important role in stabilizing the membrane both physically and structurally. Such variations in glycolipid content and composition of S. cerevisiae cells may represent an adaptive response to ethanol stress.

Cerebrosides↗
PubMed1999

Regulation of insulin-stimulated glucose transport by chronic glucose exposure in 3T3-L1 adipocytes.

Chronic hyperglycemia causes insulin resistance, termed glucose toxicity. Herein we studied chronic glucose-dependent regulation of the glucose transport system in adipocytes. 3T3-L1 adipocytes were incubated for up to 24 h with low (1 mM) or high (25 mM) glucose, and glucose transport was subsequently analyzed. 100 nM insulin was present throughout the experiments. 24 h incubation with 1 mM glucose caused a 2.3+/-0.4 fold increase in glucose transport activity, compared to the values obtained with 25 mM glucose. This difference was not observed when 24 h incubation was carried out without insulin. Glucose transport activity was not increased at 3 or 6 h incubation with 1 mM glucose, but was increased at 12 h, which closely paralleled increased expression of GLUT1. In addition to increased GLUT1 expression, more efficient translocation of GLUT1 to the plasma membrane was observed when incubated with 1 mM glucose compared to 25 mM glucose. The addition of azaserin or deprivation of glutamine at 25 mM glucose did not increase the glucose transport activity to the level obtained with 1 mM glucose. PD98059 did not affect glucose transport activity when incubated with 1 mM or 25 mM glucose. In conclusion, the present study is the first to show that, in 3T3-L1 adipocytes, chronic exposure to low (1 mM) and high (25 mM) glucose leads to different insulin-stimulated glucose transport activities. These differences result from the difference in the expression and plasma membrane distribution of GLUT1, but not of GLUT4, and the hexosamine biosynthesis pathway or extracellular signal-regulated protein kinase is not involved.

3T3 Cells↗
PubMed1981

Studies on the polydispersity and heterogeneity of proteokeratan sulfate from calf and porcine cornea.

After proteolysis of the calf and porcine corneae with papain 66 (calf) and 56 (hog) polysaccharide-containing fractions were obtained by chromatography on Dowex 1X2 and fractionating precipitation with ethanol (calf) and by chromatography on Dowex 1X2 and CPC-cellulose (hog). The sulfatation degrees (mol sulfate/mol hexosamine) and molecular weights (Mw) of 13 peptidokeratan sulfate fractions from calf cornea and of 9 such fractions from porcine cornea were 0.41-1.25 (Mw 3200-21 500), and 0.42-1.41 (Mw = 4900-25 600), respectively. It was found that the sulfatation degree increases more than proportionally with the chain-length. More than 90% of total keratan sulfate in both cases contain 2-3 mannose and 5-9 amino acid molecules per peptidokeratan sulfate molecule. About 30% of the corepeptide amino acids were asparagine or aspartic acid. More than 90% of the peptidokeratan sulfates from porcine cornea exhibits chain lengths of 31-47 disaccharide units. Two oligosaccharide peptides were isolated from porcine cornea, both being sulfate-free. Besides a core peptide of about 9 amino acids (2 Asx) one of them showed a sugar composition very similar to that of the binding-region from corneal keratan sulfate accord. to Keller, R., Stein, T., Stuhlsatz, H.W., Greiling, H., Ohst, E., Müller, E., & Scharf, H.-D. (1981) Hoppe-Seyler's Z. Physiol. Chem. 362, 327-336: 3 Man, 2 Gal, 4 GlcNAc. The calculated molecular weight based on 3 mannose residues (Mw = 2 600) agrees with that determined by gel chromatography. The second oligosaccharide peptide was homogeneous on electrophoresis and contained the constituents of the linkage region from chondroitin sulfate beside those from keratan sulfate. Based on 4 mannose residues the calculated molecular weight (4 300) is in agreement with that from gel chromatography. The sequence Asn-X-Asx starting with the binding-Asn is postulated in the core protein of proteokeratan sulfate from amino acid analyses of the corneal peptidokeratan sulfate fractions.

Amino Acid Sequence↗
PubMed1998

Malonyl CoA, long chain fatty acyl CoA and insulin resistance in skeletal muscle.

Malonyl CoA is an inhibitor of carnitine palmitoyl transferase 1 (CPT1), the enzyme that regulates the transfer of long chain fatty acyl CoA into mitochondria. By virtue of this effect, it is thought to play a key role in regulating fatty acid oxidation. Thus, when the supply of glucose to muscle is increased, malonyl CoA levels increase in keeping with a decreased need for fatty acid oxidation, and fatty acids are preferentially esterified to form diaglycerol and triglycerides. In contrast, during exercise, when the need for fatty acid oxidation is increased, malonyl CoA levels fall. Changes in glucose supply regulate malonyl CoA by modulating the concentration of cytosolic citrate, an allosteric activator of acetyl CoA carboxylase (ACC), the rate-limiting enzyme for malonyl CoA formation and a precursor of its substrate cytosolic acetyl CoA. Conversely, exercise lowers the concentration of malonyl CoA, by activating an AMP-activated protein kinase, which phosphorylates and inhibits ACC. A number of reports have linked sustained increases in the concentration of malonyl CoA in muscle to insulin resistance. In this paper, we review these reports, as well as the notion that changes in malonyl CoA contribute to the increases in long chain fatty acyl CoA, (LCFA CoA), diacylglycerol and triglyceride content and changes in protein kinase C activity and distribution observed in insulin-resistant muscle. We also review the implications of the malonyl CoA/LCFA CoA hypothesis to two other proposed mechanisms for insulin resistance, the glucose-fatty acid cycle and the hexosamine theory.

Acyl Coenzyme A↗