16 results on '"Sano, N."'
Search Results
2. Biliary excretion of sulfated bile acids and organic anions in zone 1- and zone 3-injured rats.
- Author
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Sasamoto T, Sano N, and Takikawa H
- Subjects
- ATP-Binding Cassette Transporters metabolism, Animals, Biological Transport, Bromobenzenes, Chemical and Drug Induced Liver Injury, Liver pathology, Liver Diseases pathology, Male, Phenolphthaleins pharmacokinetics, Pravastatin pharmacokinetics, Propanols, Rats, Rats, Sprague-Dawley, Taurolithocholic Acid analogs & derivatives, Taurolithocholic Acid pharmacokinetics, Anions, Bile metabolism, Bile Acids and Salts pharmacokinetics, Biliary Tract metabolism, Liver metabolism, Liver Diseases metabolism
- Abstract
Background and Aims: There are several reports on the biliary excretion of bile acids and organic anions in zone 1- and zone 3-injured rat liver, but the results are controversial. In order to dissolve the discrepancy between previous works about the role of hepatic zonation on the hepatic handling of the substrates of multidrug resistance protein 2, the biliary excretion of sulfated bile acids, pravastatin and phenolphthalein glucuronide was studied in zone 1- and zone 3-injured rats., Methods: Zone 1 and zone 3 injury were caused by allyl alcohol and bromobenzene, respectively. Bile acid sulfates, pravastatin and phenolphthalein glucuronide were administered i.v. to bile duct-cannulated rats, and their biliary excretion was studied., Results: The biliary excretion of a tracer dose of taurolithocholate-3-sulfate and its excretory maximum were unchanged in zone 1 injury, but were diminished in zone 3 injury, whereas the biliary excretion of taurochenodeoxycholate-3-sulfate was unchanged in zone 1 and zone 3 injury. The biliary excretion of pravastatin and phenolphthalein glucuronide was markedly decreased only in zone 3 injury, whereas the excretory maximum of phenolphthalein glucuronide was decreased in both zone 1 and zone 3 injury., Conclusions: These findings indicate that zone 3 is important for the biliary excretion of substrates of multidrug resistance protein 2.
- Published
- 2006
- Full Text
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3. Biliary excretion of taurocholate, organic anions and vinblastine in rats with alpha-naphthylisothiocyanate-induced cholestasis.
- Author
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Kurihara H, Sano N, and Takikawa H
- Subjects
- 1-Naphthylisothiocyanate administration & dosage, 1-Naphthylisothiocyanate toxicity, Administration, Oral, Animals, Anions, Biological Transport drug effects, Cholestasis chemically induced, Disease Models, Animal, Male, Rats, Rats, Sprague-Dawley, Antineoplastic Agents, Phytogenic pharmacokinetics, Bile metabolism, Bile Acids and Salts metabolism, Cholagogues and Choleretics pharmacokinetics, Cholestasis metabolism, Taurocholic Acid pharmacokinetics, Vinblastine pharmacokinetics
- Abstract
Background and Aims: alpha-Naphthylisothiocyanate (ANIT) is known to cause cholestasis due to injury of the bile duct epithelial cells. The aim of the present study was to examine the effect of a single dose of ANIT on the biliary excretion of various cholephilic compounds and on the amount of canalicular transporters., Methods: Twenty-four hours after the oral administration of ANIT (100 mg/kg), the biliary excretion of taurocholate, leukotriene C(4), pravastatin and vinblastine was studied. The protein levels of the bile salt export pump and multidrug resistance protein 2 and the immunostaining of multidrug resistance protein 2 in the liver were also examined., Results: The ANIT treatment markedly decreased the biliary excretion of tracer amounts of taurocholate, leukotriene C(4), pravastatin and vinblastine. The biliary excretory maximum of taurocholate was also markedly decreased after ANIT treatment. The ANIT treatment had no effect on the protein levels of bile salt export pump and multidrug resistance protein 2 and the immunostaining of multidrug resistance protein 2 in the liver., Conclusions: These findings support canalicular transporters having little effect on the marked impairment of biliary excretion of cholephilic compounds in ANIT-induced cholestasis., ((c) 2005 Blackwell Publishing Asia Pty Ltd.)
- Published
- 2005
- Full Text
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4. Biliary excretion of olmesartan, an anigotensin II receptor antagonist, in the rat.
- Author
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Takayanagi M, Sano N, and Takikawa H
- Subjects
- ATP-Binding Cassette Transporters physiology, Animals, Cephalosporins pharmacology, Common Bile Duct drug effects, Male, Olmesartan Medoxomil, Phenothiazines pharmacology, Pravastatin pharmacology, Rats, Rats, Mutant Strains, Rats, Sprague-Dawley, Sulfobromophthalein pharmacology, Taurochenodeoxycholic Acid pharmacology, Taurocholic Acid pharmacology, Vinblastine pharmacology, Angiotensin II Type 1 Receptor Blockers pharmacokinetics, Common Bile Duct metabolism, Imidazoles pharmacokinetics, Tetrazoles pharmacokinetics
- Abstract
Background and Aim: Olmesartan (RNH-6270) is a newly developed anigotensin II receptor antagonist, and has been reported to be excreted into feces. To examine the mechanism of the biliary excretion of olmesartan, we studied its biliary excretion in rats., Methods: The biliary excretion of olmesartan in Eisai hyperbilirubinemic rats (EHBR), a multidrug resistance protein 2-deficient rat, was compared with control rats, and the effect of organic anions and cation and bile acids on the biliary excretion of olmesartan was studied in control rats., Results: The biliary excretion of olmesartan was markedly delayed in EHBR. The biliary excretion of olmesartan was inhibited by sulfobromophthalein, cefpiramide and pravastatin, but was not inhibited by taurocholate or tauroursodeoxycholate. Vinblastine inhibited and phenothiazine treatment increased the biliary excretion of olmesartan., Conclusions: These findings suggest that olmesartan is excreted into the bile mainly by multidrug resistance protein 2 and partly by P-glycoprotein.
- Published
- 2005
- Full Text
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5. Effects of colchicine on the maximum biliary excretion of cholephilic compounds in rats.
- Author
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Tachizawa H, Sano N, and Takikawa H
- Subjects
- ATP Binding Cassette Transporter, Subfamily B, Member 1 pharmacokinetics, Analysis of Variance, Animals, Bile drug effects, Erythromycin pharmacokinetics, Indocyanine Green pharmacokinetics, Male, Rats, Rats, Sprague-Dawley, Sulfobromophthalein pharmacokinetics, Taurochenodeoxycholic Acid pharmacokinetics, Taurocholic Acid pharmacokinetics, Taurolithocholic Acid pharmacokinetics, Bile metabolism, Bile Acids and Salts metabolism, Colchicine pharmacology
- Abstract
Background and Aim: Colchicine, an inhibitor of intracellular vesicular transport, has been reported to inhibit the biliary excretion of bile acids and organic anions, but the previous findings are controversial. In order to systematically evaluate the effect of colchicine on the biliary excretion of cholephilic compounds, we studied the effect of colchicine on the biliary excretion of substrates of various canalicular transporters, which were administered at or above the excretory maximum in rats., Methods: Substrates of various canalicular adenosine triphosphate-binding-cassette transporters were infused at or above the rate of maximum excretion into rats, and the effect of colchicine (0.2 mg/100 g), which was intraperitoneally injected 3 h before, on the biliary excretion was studied. Furthermore, the effect of tauroursodeoxycholate (TUDC) co-infusion on the biliary excretion of taurocholate (TC) after colchicine treatment was also studied., Results: The biliary excretion of TC and cholate administered at the rate of 1 micro mol/min/100 g was markedly inhibited by colchicine, whereas that of TUDC was not inhibited even with the infusion rate of 2 micro mol/min/100 g. TUDC co-infusion at the rate of 1 micro mol/min/100 g increased the biliary excretion of TC (1 micro mol/min/100 g), which was decreased by the colchicine pretreatment. The biliary excretory maximum of taurolithocholate-sulfate and sulfobromophthalein, substrates of the multidrug resistance protein 2, of erythromycin, a substrate of the P-glycoprotein, and of indocyanine green were not affected by colchicine., Conclusions: The different excretory maximums of TC and TUDC and the different effect of colchicine on the excretion of these bile acids are considered to be a result of different regulatory mechanisms of vesicular targeting of the bile salt export pump to the canalicular membrane by these bile acid conjugates. The vesicular targeting of the multidrug resistance protein 2 and the P-glycoprotein to the canalicular membrane is considered to be colchicine insensitive in the absence of bile acid coadministration.
- Published
- 2004
- Full Text
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6. Biliary excretion of azelnidipine, a calcium antagonist, in rats.
- Author
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Hanawa N, Sano N, and Takikawa H
- Subjects
- Animals, Azetidinecarboxylic Acid antagonists & inhibitors, Cholagogues and Choleretics pharmacology, Dihydropyridines antagonists & inhibitors, Male, Multidrug Resistance-Associated Protein 2, Rats, Rats, Sprague-Dawley, Sulfobromophthalein pharmacology, Taurocholic Acid pharmacology, Vinblastine pharmacology, Azetidinecarboxylic Acid analogs & derivatives, Azetidinecarboxylic Acid metabolism, Bile metabolism, Calcium Channel Blockers metabolism, Dihydropyridines metabolism, Hyperbilirubinemia metabolism, Membrane Transport Proteins deficiency, Multidrug Resistance-Associated Proteins deficiency
- Abstract
Background and Aims: Azelnidipine (CS-905) is a novel dihydropyridine calcium antagonist that is known to be excreted in feces. To examine the mechanism of biliary excretion of azelnidipine, the authors studied its biliary excretion in Eisai hyperbilirubinuria rats (EHBR), multidrug resistance protein (Mrp)2-deficient rats, and the effect of cholephilic compounds on the biliary excretion of azelnidipine in rats., Methods: Radiolabeled azelnidipine was intravenously administered to EHBR and control rats, and the biliary excretion of radiolabeled metabolites was studied. Furthermore, the effect of sulfobromophthalein, taurocholate and vinblastine on the biliary excretion of azelnidipine metabolites was also studied in control rats., Results: The biliary excretion of azelnidipine metabolites was delayed in EHBR. The biliary excretion of azelnidipine metabolites was inhibited by sulfobromophthalein and vinblastine, but was not inhibited by taurocholate or phenothiazine pretreatment., Conclusion: These findings suggest that the metabolites of azelnidipine are excreted into the bile partly by Mrp2 and P-glycoprotein.
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- 2004
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7. Effects of lipopolysaccharide on the biliary excretion of bile acids and organic anions in rats.
- Author
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Hojo M, Sano N, and Takikawa H
- Subjects
- Animals, Anions, Male, Rats, Rats, Sprague-Dawley, Statistics, Nonparametric, Taurine chemistry, Bile metabolism, Bile Acids and Salts metabolism, Lipopolysaccharides pharmacology
- Abstract
Background: Lipopolysaccharide is known to be a cause of cholestasis associated with sepsis. It has also recently been reported to down-regulate the basolateral and canalicular transporters. The aim of the present study was to examine simultaneously the effect of lipopolysaccharide on the biliary excretion of typical substrates of bile salt export pump and multidrug resistance protein 2 in vivo, and the effect of lipopolysaccharide on the amount of these transporters., Methods: After intravenous administration of O127:B8-derived lipopolysaccharide (2.5 mg/kg), the biliary excretion of taurocholate and various organic anions was studied, and the protein levels of bile salt export pump and multidrug resistance protein 2 in the crude liver membrane was determined by western blot analysis., Results: Lipopolysaccharide decreased the biliary excretion of tracer amounts of taurocholate, leukotriene C4, taurolithocholate-3-sulfate and temocapril without affecting bile flow. The biliary excretion of high doses of taurocholate and sulfobromophthalein was markedly inhibited by lipopolysaccharide. Lipopolysaccharide decreased bile salt export pump levels in the liver plasma membrane fraction to 48% of control rats, and markedly decreased multidrug resistance protein 2 levels to 17% of control rats., Conclusions: These findings support the hypothesis that down-regulation of the canalicular transporters by lipopolysaccharide causes the impairment of the biliary excretion of bile acids and organic anions in cholestasis of sepsis prior to the decrease of bile flow., (Copyright 2003 Blackwell Publishing Asia Pty Ltd)
- Published
- 2003
- Full Text
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8. Inhibition of ileal bile acid absorption by colestimide.
- Author
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Takeuchi A, Sano N, and Takikawa H
- Subjects
- Animals, Anion Exchange Resins administration & dosage, Epichlorohydrin, Imidazoles, Male, Rats, Rats, Sprague-Dawley, Resins, Synthetic, Anion Exchange Resins pharmacology, Bile Acids and Salts pharmacokinetics, Ileum metabolism, Intestinal Absorption drug effects
- Abstract
Background: Colestimide is a new type of anion-exchange resin in Japan, but its effect on bile acid absorption in the ileum has not been studied., Methods: Absorption of ursodeoxycholate, tauroursodeoxycholate, cholate, taurocholate and taurolithocholate-sulfate in rat ileum was compared in the presence and absence of colestimide. Bile acid adsorption by colestimide in vitro was also studied., Results: All bile acids were efficiently absorbed by the ileum, and the cumulative absorption during 60 min was 25-78%. The absorption of ursodeoxycholate, tauroursodeoxycholate and taurocholate was inhibited by colestimide, whereas that of cholate and taurolithocholate-sulfate was not inhibited by colestimide. Adsorption of bile acids by colestimide in vitro was higher with taurine conjugates than with the unconjugated forms., Conclusions: Colestimide was shown to be useful to inhibit the physiologically important ileal absorption of bile acid amides in vivo., (Copyright 2003 Blackwell Publishing Asia Pty Ltd)
- Published
- 2003
- Full Text
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9. Effect of colestimide on absorption of unconjugated bile acids in the rat jejunum.
- Author
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Onishi T, Sano N, and Takikawa H
- Subjects
- Animals, Anion Exchange Resins metabolism, Bile Acids and Salts pharmacokinetics, Cholic Acid pharmacokinetics, Epichlorohydrin, Imidazoles, Male, Rats, Rats, Sprague-Dawley, Resins, Synthetic, Time Factors, Anion Exchange Resins pharmacology, Deoxycholic Acid pharmacokinetics, Intestinal Absorption drug effects, Jejunum metabolism
- Abstract
Background: Colestimide is a newly developed bile acid-binding resin in Japan, but its bile acid-binding properties have not been studied., Methods: The absorption of unconjugated bile acids (5 mmol/L) in the ligated rat jejunum was compared in the presence and absence of colestimide. Furthermore, bile acid adsorption by colestimide was also studied in vitro., Results: All bile acids were efficiently absorbed in the jejunum and the cumulative absorption during 120 min was 29-63%. The absorption of chenodeoxycholate, lithocholate, deoxycholate and ursodeoxycholate was dose-dependently inhibited by 2.5 and 5 mg colestimide, whereas the absorption of cholate was not inhibited, even in the presence of 5 mg colestimide. Adsorption of bile acids by colestimide in vitro was approximately 60% for chenodeoxycholate, lithocholate, deoxycholate and ursodeoxycholate, whereas the adsorption of cholate was low (16%)., Conclusions: Jejunal absorption of ursodeoxycholate was inhibited by colestimide to a similar extent as other dihydroxy bile acids, whereas that of cholate was not inhibited under the same conditions.
- Published
- 2002
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10. Serum amino-terminal propeptide of type III procollagen and 7S domain of type IV collagen correlate with hepatic iron concentration in patients with chronic hepatitis C following alpha-interferon therapy.
- Author
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Shimizu I, Omoya T, Takaoka T, Wada S, Wada H, Taoka M, Hayashi H, Hayashi S, Honda H, Sano N, and Ito S
- Subjects
- Adult, Female, Humans, Hyaluronic Acid blood, Male, Middle Aged, Protein Structure, Tertiary, Collagen blood, Hepatitis C, Chronic drug therapy, Interferon-alpha therapeutic use, Iron analysis, Liver chemistry, Procollagen blood
- Abstract
Background: It has been reported that chronic infection with hepatitis C virus is associated with excess iron deposits in the liver of subjects who are neither alcoholics nor recipients of blood transfusions. However, little is known about the relationship between hepatic iron concentration (HIC) and the serum levels of hepatic fibrogenesis markers, which were caused by interferon therapy for chronic hepatitis C. Therefore, changes in the serum amino-terminal propeptide of type III procollagen (P-III-P) and the 7S domain of type IV collagen (7S-IV) in 16 patients treated with alpha-interferon (IFN-alpha) were studied, and their HIC and histological assessment evaluated. Hepatic iron concentrations were measured by using liver biopsy specimens obtained before and 6 months after the cessation of treatment., Methods and Results: Eight subjects (50%) who had normal alanine transaminase levels at 6 months after therapy showed significantly lowered HIC, and attenuated hepatic iron staining with decreased serum levels of P-III-P and 7S-IV compared to the remaining subjects. The HIC was significantly correlated with the serum levels of P-III-P and 7S-IV in all subjects., Conclusions: These findings suggest that IFN-alpha treatment may decrease stimuli for fibrogenesis, at least in part, by reducing the hepatic iron deposition in patients with chronic hepatitis C.
- Published
- 2001
- Full Text
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11. Effects of colchicine and phenothiazine on biliary excretion of organic anions in rats.
- Author
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Takikawa H, Sano N, Akimoto K, Ogasawara T, and Yamanaka M
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- Animals, Bile drug effects, Coloring Agents pharmacokinetics, Dinitrochlorobenzene metabolism, Glutathione metabolism, Indocyanine Green pharmacokinetics, Male, Rats, Rats, Sprague-Dawley, Sulfobromophthalein pharmacokinetics, ATP Binding Cassette Transporter, Subfamily B, Member 1 physiology, Bile metabolism, Colchicine pharmacology, Phenothiazines pharmacology
- Abstract
Vesicular transport inhibitors have been reported to inhibit biliary excretion of some organic anions, suggesting that vesicular transport has a role in intracellular transport of these compounds. However, these inhibitors are substrates for P-glycoprotein. To examine whether P-glycoprotein has a role in canalicular transport of organic anions in addition to the canalicular multispecific organic anion transporter, we studied the effect of colchicine, a vesicular transport inhibitor, and phenothiazine to increase P-glycoprotein expression on biliary excretion of various organic anions in rats. Colchicine treatment slightly but significantly inhibited biliary excretion of indocyanine green, dinitrophenyl-glutathione and pravastatin, and had no effect on biliary excretion of sulphobromophthalein and dibromosulphophthalein. Phenothiazine treatment did not affect biliary excretion of indocyanine green and pravastatin, but it increased biliary sulphobromophthalein-glutathione excretion. In conclusion, the present findings suggest that P-glycoprotein plays an additive role on biliary excretion of some organic anions in addition to the canalicular multispecific organic anion transporter.
- Published
- 1998
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12. Changes in biliary excretory mechanisms in rats with ethinyloestradiol-induced cholestasis.
- Author
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Takikawa H, Takamori Y, Sano N, Kuyama Y, and Yamanaka M
- Subjects
- Animals, Bile chemistry, Biological Transport, Cholestasis chemically induced, Estradiol Congeners, Ethinyl Estradiol, Male, Rats, Rats, Sprague-Dawley, Bile metabolism, Bile Acids and Salts metabolism, Cholestasis metabolism
- Abstract
Several excretory pathways for cholephilic compounds have been known. To examine the changes in excretory pathways in cholestasis induced by ethinyloestradiol, various bile acids, organic anions and organic cations were intravenously administered to ethinyloestradiol-treated rats and their biliary excretion was studied. Biliary excretion of taurocholate was slightly delayed, but its excretory maximum was markedly decreased. Biliary excretion of lithocholate-3-O-glucuronide, leukotriene C4, sulphobromophthalein and pravastatin was markedly impaired to a similar extent. Biliary excretion of vinblastine, a P-glycoprotein substrate, was increased, suggesting increased expression of P-glycoprotein. In contrast, biliary excretion of erythromycin, a cationic antibiotic, was markedly impaired. In conclusion, ethinyloestradiol treatment altered the biliary excretion of organic compounds, which may partly be related to changes of the canalicular transporters.
- Published
- 1998
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13. Absorption of unconjugated bile acids and tauroursodeoxycholate in the rat intestine.
- Author
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Takikawa H, Yokote M, Sano N, Kuyama Y, and Yamanaka M
- Subjects
- Animals, Intestinal Absorption physiology, Ligation, Male, Perfusion, Rats, Rats, Sprague-Dawley, Time Factors, Ursodeoxycholic Acid metabolism, Bile Acids and Salts metabolism, Ileum metabolism, Jejunum metabolism, Taurochenodeoxycholic Acid metabolism
- Abstract
The absorption of ursodeoxycholate and its tauro-conjugate by the jejunum and the terminal ileum of rat intestine was compared with that of other unconjugated bile acids and taurocholate. In the ligated jejunum, the efficacy of absorption of unconjugated bile acids was in the following order: ursodeoxycholate = deoxycholate > chenodeoxycholate = cholate > lithocholate. This order cannot be explained by the theory that the passive diffusion of bile acids is faster the less hydroxyl bonds in the molecule. These findings on the unconjugated bile acids in the ligated jejunum were further confirmed by perfusion experiments. In the ligated terminal ileum, ursodeoxycholate, cholate and deoxycholate were absorbed as fast as taurocholate or tauroursodeoxycholate, whereas absorption of chenodeoxycholate was significantly slower. The Na+-dependency of the absorption of ursodeoxycholate and cholate in the terminal ileum was confirmed by perfusion studies. In conclusion, intestinal absorption of ursodeoxycholate was efficient in both the jejunum and ileum and these results may contribute to the high availability of ursodeoxycholate in various hepatobiliary diseases.
- Published
- 1997
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14. Effect of taurolithocholate-3-sulphate on biliary excretion of sulphobromophthalein and dibromosulphophthalein in the Eisai hyperbilirubinaemic rat.
- Author
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Takikawa H, Sano N, Sato A, and Yamanaka M
- Subjects
- Animals, Chromatography, Thin Layer, Male, Rats, Rats, Sprague-Dawley, Taurolithocholic Acid pharmacology, Time Factors, Bile metabolism, Hyperbilirubinemia metabolism, Sulfobromophthalein metabolism, Taurolithocholic Acid analogs & derivatives
- Abstract
We previously reported that biliary lithocholate-3-sulphate excretion was inhibited by dibromosulphophthalein, not by sulphobromophthalein in Eisai hyperbilirubinaemic rats (EHBR); instead its excretion was inhibited by both organic anions in control rats. In the present study, the effect of taurolithocholate-3-sulphate on the excretion of sulphobromophthalein and dibromosulphophthalein was studied in EHBR and control Sprague-Dawley rats. Taurolithocholate-3-sulfate infusion inhibited biliary excretion of sulphobromophthalein and dibromosulphophthalein in both EHBR and control rats. These findings indicate that in control rats biliary excretion of taurolithocholate-3-sulphate is mediated by a carrier common for both organic anions, and that in EHBR, in which the canalicular multispecific organic anion transporter is impaired, the excretory pathway for taurolithocholate-3-sulphate is also partly identical to that for both organic anions.
- Published
- 1997
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15. Effect of tauro-alpha-muricholate and tauro-beta-muricholate on oestradiol-17 beta-glucuronide-induced cholestasis in rats.
- Author
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Takikawa H, Sano N, Aiso M, Takamori Y, and Yamanaka M
- Subjects
- Animals, Isomerism, Male, Rats, Rats, Sprague-Dawley, Taurocholic Acid pharmacology, Cholestasis chemically induced, Cholestasis prevention & control, Estradiol analogs & derivatives, Taurochenodeoxycholic Acid pharmacology, Taurocholic Acid analogs & derivatives
- Abstract
The effect of tauro-beta-muricholate (beta MC-tau) and tauro-alpha-muricholate (alpha MC-tau) on oestradiol-17 beta-glucuronide (E217G)-induced cholestasis was compared with that of tauroursodeoxycholate (UDC-tau) in rats. Like UDC-tau, alpha MC-tau and beta MC-tau infused at the rate of 0.2 mumol/min per 100 g bodyweight (BW) completely inhibited the cholestasis induced by E217G infused at the rate of 0.06 mumol/min per 100 g BW for 20 min. These findings indicate that beta MC-tau and alpha MC-tau are useful in protecting against various types of experimental cholestasis, as well as against bile acid-induced cholestasis.
- Published
- 1997
- Full Text
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16. Intestinal absorption of lithocholate and its sulfate and glucuronide in rats.
- Author
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Takikawa H, Yokote M, Sano N, Nakaki M, and Yamanaka M
- Subjects
- Absorption, Animals, Cholagogues and Choleretics pharmacokinetics, Ileum diagnostic imaging, Jejunum diagnostic imaging, Male, Perfusion, Radioisotopes, Radionuclide Imaging, Rats, Rats, Sprague-Dawley, Taurocholic Acid pharmacokinetics, Glucuronates pharmacokinetics, Ileum metabolism, Jejunum metabolism, Lithocholic Acid analogs & derivatives, Lithocholic Acid pharmacokinetics
- Abstract
The absorption of lithocholate and its sulfate and glucuronide in rat jejunum and terminal ileum was studied. Tracer amounts of radiolabelled bile acids were administered to the ligated intestinal segments, and their absorption was monitored by biliary excretion through a bile duct catheter. Absorption of lithocholate was faster in the terminal ileum than in the jejunum. Although the sulfation reduced lithocholate absorption in the jejunum, it did not affect lithocholate absorption in the terminal ileum. This was due to the Na+-dependency of ileal absorption of lithocholate-sulfate assessed by perfusion studies. In contrast, the glucuronidation markedly reduced lithocholate absorption both in the jejunum and the terminal ileum. These findings indicate that the glucuronidation is more effective than sulfation in detoxifying lithocholate as far as the prevention of its intestinal absorption is concerned.
- Published
- 1995
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