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Biomedical subjects

H Oura

Publications and source records attributed to H Oura.

At least 73 records · Page 4Linked to original sources
PubMed1991

Improvement of hyperglycemia and hyperlipemia in streptozotocin-diabetic rats by a methanolic extract of Prunus davidiana stems and its main component, prunin.

Blood glucose and total lipid levels in rats with streptozotocin-induced diabetes were determined after intraperitoneal administration of a methanolic extract of Prunus davidiana Fr. stems and its main component, prunin (= naringenin 7-O-beta-D-glucoside). From the data obtained it was concluded that intraperitoneal administration of the methanolic extract and prunin produced a significant hypoglycemic effect. Total blood lipids were also decreased by these substances. Thus, it is suggested that this methanolic extract contains one or more hypoglycemic principles including the main flavanone glycoside, prunin, which can significantly reduce the levels of blood glucose and total lipids in streptozotocin-diabetic rats.

Animals↗
PubMed1991

Effects of ginsenoside-Rb2 on adenine nucleotide content of rat hepatic tissue.

In comparison with non-diabetic rats, the tissue ATP content of diabetic rats is lower and the AMP content higher. However, daily intraperitoneal administration of ginsenoside-Rb2 for several days resulted in an increase of tissue ATP content and a decrease of AMP content, characterized by an increase in the adenine nucleotide content, as well as improvement of energy charge. Thus, ginsenoside-Rb2 administration caused a change in the pattern of metabolism, activating the ATP supply system.

Adenine Nucleotides↗
PubMed1991

Augmentation of renal response by magnesium lithospermate B.

Magnesium lithospermate B and adenine were given simultaneously to rats p.o. in order to investigate their renal effects. In rats given magnesium lithospermate B at a dose of 5 mg/kg body weight/day for 12 or 24 days, glomerular filtration rate, renal plasma flow and renal blood flow were increased significantly. A significant increase in renal function parameters was also found in rats given 10 mg of magnesium lithospermate B. Urinary excretion of prostaglandin E2 was increased by administration of magnesium lithospermate B, while those of 6-keto-prostaglandin F1 alpha and thromboxane B2 were unaffected at a dose of 5 mg or 10 mg/kg body weight/day for 12 or 24 days. The activity of kallikrein in urine increased markedly and significantly in rats given 5 or 10 mg of magnesium lithospermate B for 12 or 24 days. From these results, it seems that magnesium lithospermate B increases renal function by improving the renal circulatory state through activation of kallikrein and promotion of prostaglandin E2 production.

Administration, Oral↗
PubMed1991

Production of methylguanidine from creatinine via creatol by active oxygen species: analyses of the catabolism in vitro.

The chemical oxidative conversion of creatinine (Cr) into methylguanidine (MG) has been followed by 1H-NMR and HPLC. By using active oxygen species generated by Fenton's reagent (Fe2+ and H2O2) or the similar reagent (Fe3+ and H2O2), creatol (CTL), a metabolite newly isolated from the urine of uremic patients, and creatones A and B were experimentally detected in the reaction mixture and implicated as successive intermediates in the pathway from CR to MG. An alternative oxidation of Cr to demethylcreatinine (glycocyamidine) was also observed. The importance of CTL in this in vitro oxidation mechanism is discussed.

Chromatography, High Pressure Liquid↗
PubMed1991

Studies on the precursor of methylguanidine in rats with renal failure.

Each of creatinine (Cr), guanidinoacetic acid (GAA) and arginine (Arg) was administered intraperitoneally to rats with renal failure, and the levels of methylguanidine (MG) in the serum, liver, kidney, muscle and urine were determined at certain intervals. The levels of MG in the serum, liver, kidney, muscle and urine after Cr administration increased markedly with time. The amount of total MG at 24 h was estimated to be 114 micrograms/100 g body weight, which accounted for 0.46% of the Cr dose. In contrast, changes in MG levels after administration of GAA or Arg were only slight in comparison with those after Cr administration. Thus, MG was proved to be produced mainly from Cr.

Animals↗
PubMed1991

Effects of rhubarb tannins on uremic toxins.

The effects of each of several tannins purified from Rhei Rhizoma on serum constituents were investigated in rats with adenine-induced renal failure. Blood levels of urea nitrogen, methylguanidine (MG), and guanidinosuccinic acid (GSA) were significantly decreased in rats given (-)-epicatechin 3-O-gallate at a dose of 2.5, 5 or 10 mg/kg body weight/day for 24 days. The creatinine (Cr) level was also significantly decreased in rats given 5 and 10 mg of this compound. A significant decrease in urea nitrogen, MG, and GSA was found in rats given 6.25 mg of procyanidin B-2 3,3'-di-O-gallate. However, unlike the former two components the administration of 12.5 mg of procyanidin C-1 3,3',3''-tri-O-gallate produced a considerable or significant increase in bLood levels of urea nitrogen, Cr, MG, and GSA. RG-tannin had a weaker overall effect on serum constituents except for GSA in comparison with the corresponding effect of (-)-epicatechin 3-O-gallate and 6.25 mg of procyanidin B-2 3,3'-di-O-gallate. Rhatannin tended to increase the serum nitrogen constituents.

Animals↗
PubMed1991

Potentiating effect of converting enzyme inhibitor captopril to the renal responses of magnesium lithospermate B in rats with adenine-induced renal failure.

The renal responses of magnesium lithospermate B were investigated in the presence or absence of pretreatment with the converting enzyme (kininase II) inhibitor, captopril, in rats with adenine-induced renal failure. Magnesium lithospermate B (10 mg/kg body weight) caused a marked increase in the levels of the renal functional parameters (glomerular filtration rate, renal plasma flow and renal blood flow), accompanied by significant increases in urinary excretions of prostaglandin E2 (PGE2), kallikrein, sodium and creatinine. The administration of magnesium lithospermate B in combination with captopril (2 mg/kg body weight, 2 times) caused a further increase in renal functional parameters, urinary sodium and creatinine excretions. However, the kallikrein activity was similar to the control level. There were no significant changes between urinary PGE2 following magnesium lithospermate B alone, or in combination with captopril. In addition, angiotensin converting enzyme activity did not change following the administration of magnesium lithospermate B alone, but was significantly decreased in rats given captopril, both alone and in combination with magnesium lithospermate B. The captopril administration group (captopril alone or in combination with magnesium lithospermate B) showed a significant decrease in blood pressure. From these results, it seems that the combination of magnesium lithospermate B and captopril induces a further increase in renal function by improving the renal circulatory state.

Adenine↗
PubMed1990

Renal responses to magnesium lithospermate B.

Renal responses to magnesium lithospermate B isolated from Salviae miltiorrhizae radix were examined in normal rats. Urinary sodium, potassium, prostaglandin E2 and kallikrein excretion was significantly increased after magnesium lithospermate B administration, whereas excretion of urinary 6-keto-prostaglandin F1 alpha and thromboxane B2 was unchanged. Rats administered with the drug also revealed a slight elevation of plasma renin activity and the levels of angiotensins I and II. Plasma aldosterone was decreased slightly. No significant changes were observed in angiotensin-converting enzyme or blood pressure.

Animals↗
PubMed1990

Production of methylguanidine from creatinine in normal rats and rats with renal failure.

Creatinine (Cr) was administered intraperitoneally to both normal rats and those given adenine, and time-course changes in methylguanidine (MG) production from Cr were compared. In rats with renal failure, the accumulation of MG in the body increased gradually with time after Cr administration. In particular, the MG level in skeletal muscle was markedly high in comparison with that in serum, liver or kidney, and a high concentration of MG was still present 24 h after Cr loading. In contrast, the amount of MG excreted into urine in these rats during 24 h after Cr administration was lower than the corresponding values in normal rats. Thus, the amount of MG per rat, distributed at 24 h after intraperitoneal administration of Cr 300 mg/100 g body weight was calculated. The production of MG from Cr was found to be markedly higher in rats with adenine-induced renal failure (172.09 micrograms/100 g body weight) than in normal rats (70.30 micrograms/100 g body weight). Produced MG was mostly excreted into urine in normal rats, whereas in rats with renal failure as much as 79.1% of produced MG was accumulated in the body.

Adenine↗
PubMed1990

Magnesium lithospermate B improves renal function via the kallikrein-prostaglandin system in rats with renal failure.

The effect of magnesium lithospermate B on the renal responses of rats with renal failure was investigated in the presence and absence of pretreatment with the kallikrein inhibitor, aprotinin. Magnesium lithospermate B caused a marked increase in the levels of the renal functional parameters (glomerular filtration rate, renal plasma flow and renal blood flow), accompanied by significant increases in urinary prostaglandin excretion (increases of prostaglandin E2 and 6-keto-prostaglandin F1 alpha excretion by 82% and 36%, respectively). The urinary excretion of kallikrein was also increased following magnesium lithospermate B administration. However, pretreatment with aprotinin abolished the renal function-facilitating action of magnesium lithospermate B concomitantly with a markedly increased urinary excretion of prostaglandin E2, 6-keto-prostaglandin F1 alpha and kallikrein. These results suggest that the kallikrein-kinin-prostaglandin B.

Animals↗
PubMed1989

Comparison of toxic effects of methylguanidine, guanidinosuccinic acid and creatinine in rats with adenine-induced chronic renal failure.

Methylguanidine (MG), guanidinosuccinic acid (GSA) and creatinine (Cr), which accumulate in the body in parallel with the progress of renal failure after adenine administration, were given separately to rats in order to compare their toxicities. Food containing adenine was given to rats for 24 days to induce renal failure, and then each of the test substances was administered intraperitoneally from the following day, the survival rates of the rats being subsequently determined. Administration of MG at varying doses produced a dose-dependent decrease in the survival rate, whereas the survival curves obtained for rats given GSA or Cr indicated weak toxicity. The levels of MG, GSA or Cr accumulated in the body were extraordinarily high in surviving rats after 14 days of administration of each respective compound. The toxic effects are discussed on the basis of these results.

Adenine↗
PubMed1989

Variations in the distribution of methylguanidine with the progression of renal failure after methylguanidine loading.

Methylguanidine (MG) was intraperitoneally administered to both normal rats and those given adenine, and MG levels in the serum, liver, kidney, muscle, brain and urine were compared. The accumulation of MG in the body increased with the progression of renal failure, whereas the rate of urinary excretion of MG in rats given adenine for 30 days was lower than the corresponding values in rats given adenine for 10 and 20 days. The velocity of MG elimination from serum and tissues became lower as the period of adenine administration lengthened. In particular, the rate of MG elimination from muscle was markedly low in comparison with that from the serum, liver, kidney or brain, and a high concentration of MG was still present 24 h after MG loading. In addition, the amount of MG obtained by subtracting the total amounts detected in the serum, liver, kidney, muscle, brain and urine from the dose decreased gradually as the period of adenine administration lengthened. The MG-scavenging effect is diminished according to the progress of renal failure.

Adenine↗
PubMed1989

Contribution of prostaglandins to the renal responses to magnesium lithospermate B isolated from salviae miltiorrhizae radix.

The involvement of prostanoids in the improvement of adenine-induced renal failure in rats by magnesium lithospermate B was studied. After intraperitoneal administration of magnesium lithospermate B to renal failure rats, the levels of glomerular filtration rate, renal plasma flow and renal blood flow were increased. Urinary excretions of prostaglandin E2 (PGE2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in renal failure rats were increased by the administration of magnesium lithospermate B, while that of thromboxane B2 had no effect. Pretreatment with indomethacin abolished the improving effect of magnesium lithospermate B on renal function concomitantly with markedly suppressed urinary excretion of prostanoids. These results suggest that the increased formation of PGE2 and 6-keto-PGF1 alpha might contribute to the improvement of adenine-induced renal failure in rats by magnesium lithospermate B.

Animals↗
PubMed1989

Effect of magnesium lithospermate B on urinary excretion of arachidonate metabolites in rats with renal failure.

The effect of magnesium lithospermate B isolated from Salviae miltiorrhizae Radix on excretion of urinary arachidonate metabolites was examined in both normal rats and those given adenine. Urinary excretion of prostaglandin E2 (PGE2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) decreased while urinary thromboxane B2 (TXB2) excretion increased markedly with the progression of renal failure. Rats administered magnesium lithospermate B showed an increase of urinary PGE2 excretion at the 6th and 12th days. Excretion of 6-keto-PGF1 alpha also showed a significant increase on the 6th and 12th days in rats with renal failure induced by the administration of adenine. However, these effects were lower than the corresponding values in normal rats. In addition, urinary PGE2 and 6-keto-PGF1 alpha excretions showed no appreciable difference in rats that exhibited progressive renal failure with continuation of the adenine administration period, as shown on the 18th and 24th days. There were no significant changes in TXB2 excretion between the control and magnesium lithospermate B-treated groups throughout the experimental period.

Animals↗
PubMed1989

Isolation of a renal function-facilitating constituent from the Oriental drug, salviae miltiorrhizae radix.

An attempt was made to isolate the active component which exhibits an improving effect on renal function from Salviae Miltiorrhazae Radix (Chinese crude drug). Systematic isolation from aqueous extract of Salviae Miltiorrhizae Radix was carried out, and Compound 1 was found to be more effective than any of the other constituents in improving renal functional parameters; that is, a marked reduction of glomerular filtration rate following adenine ingestion was improved by administration of this substance. The renal plasma flow and renal blood flow were also increased in renal failure rats. On the basis of chemical and spectroscopic data, Compound 1 was shown to be identical with magnesium lithospermate B.

Animals↗
PubMed1989

Renal function and urinary prostaglandins in rats given an adenine diet.

The glomerular filtration rate (GFR), renal plasma flow (RPF) and renal blood flow (RBF) were all markedly decreased in rats given an adenine diet as the period of adenine administration lengthened. Concurrently, the urinary excretions of prostaglandin E2 (PGE2) and 6-keto-prostaglandin F1 alpha(6-keto-PGF1 alpha) decreased gradually in parallel with the renal function parameters, whereas the urinary excretion of thromboxane B2 (TXB2) increased markedly. These findings suggest the involvement of prostaglandin in the renal circulation.

6-Ketoprostaglandin F1 alpha↗