Effects of Japanese herbal medicine inchin-ko-to on endotoxin-induced cholestasis in the rat
dc.contributor.author | Pablo Arab, Juan | |
dc.contributor.author | Ramirez, Carolina | |
dc.contributor.author | Munoz, Pablo | |
dc.contributor.author | Pizarro, Margarita | |
dc.contributor.author | Solis, Nancy | |
dc.contributor.author | Riquelme, Arnoldo | |
dc.contributor.author | Arrese, Marco | |
dc.date.accessioned | 2024-01-10T12:38:37Z | |
dc.date.available | 2024-01-10T12:38:37Z | |
dc.date.issued | 2009 | |
dc.description.abstract | Background/Objective. Inchin-ko-to (ICKT) is an herbal medicine used in Japan to treat jaundice and liver fibrosis. We investigated the effect of oral ICKT supplementation on endotoxin-induced cholestasis in the rat. Material and methods. Lipopolysaccharide (LPS) injection (1 mg/kg body weight i.p.) was used as a model of sepsis-induced cholestasis. Bite flow, biliary bile salt secretion, biliary glutathione secretion and protein expression of the main hepatobiliary transporters Na(+)-taurocholate-cotransporting peptide (Ntcp), multidrug resistance protein 2 (Mrp2) and bile salt export pump (Bsep) were analyzed by conventional techniques in ICKT treated and non-treated animals. Results. Injection of LIDS induced a significant decrease of bite ftow (-24%), biliary bite salts (-40%) and glutathione excretion (-70%) as well as a significant decrease in Ntcp (-90%) and Mrp2 (-80%) protein levels. ICKT supplementation partially prevented the effects of LIPS determining a less intense reduction in bile flow (-10%), a normalization of glutathione excretion as well as a significant increase in Mrp2 protein levels to 60% of the levels observed in control animals. ICKT administration did not modify the effects of LPS on BS secretion or Ntcp protein levels. Conclusion. Our data show that oral. supplementation of ICKT partially prevents LPS-induced cholestasis by increasing Mrp2 protein levels and biliary glutathione excretion thus increasing bite salt-independent ftow. | |
dc.description.funder | Fondo Nacional De Ciencia y Tecnologia de Chile | |
dc.fechaingreso.objetodigital | 2024-05-06 | |
dc.format.extent | 6 páginas | |
dc.fuente.origen | WOS | |
dc.identifier.issn | 1665-2681 | |
dc.identifier.pubmedid | MEDLINE:19841502 | |
dc.identifier.uri | https://repositorio.uc.cl/handle/11534/77072 | |
dc.identifier.wosid | WOS:000270400300008 | |
dc.information.autoruc | Medicina;Arab JP;S/I;132745 | |
dc.information.autoruc | Medicina;Arrese M;S/I;76095 | |
dc.information.autoruc | Medicina;Pizarro M;S/I;102250 | |
dc.information.autoruc | Medicina;Riquelme A;S/I;3538 | |
dc.information.autoruc | Medicina;Solís N;S/I;102379 | |
dc.issue.numero | 3 | |
dc.language.iso | en | |
dc.nota.acceso | Sin adjunto | |
dc.pagina.final | 233 | |
dc.pagina.inicio | 228 | |
dc.publisher | MEXICAN ASSOC HEPATOLOGY | |
dc.revista | ANNALS OF HEPATOLOGY | |
dc.rights | registro bibliográfico | |
dc.subject | Inchin-ko-to | |
dc.subject | Cholestasis | |
dc.subject | Endotoxin | |
dc.subject | Genipin | |
dc.subject | BILIARY ATRESIA PATIENTS | |
dc.subject | ORGANIC ANION TRANSPORT | |
dc.subject | LIVER FIBROSIS | |
dc.subject | BILE FORMATION | |
dc.subject | EXPORT PUMP | |
dc.subject | TJ-135 | |
dc.subject | ACID | |
dc.subject | INFLAMMATION | |
dc.subject | GLUTATHIONE | |
dc.subject | MECHANISMS | |
dc.subject.ods | 03 Good Health and Well-being | |
dc.subject.odspa | 03 Salud y bienestar | |
dc.title | Effects of Japanese herbal medicine inchin-ko-to on endotoxin-induced cholestasis in the rat | |
dc.type | artículo | |
dc.volumen | 8 | |
sipa.codpersvinculados | 132745 | |
sipa.codpersvinculados | 76095 | |
sipa.codpersvinculados | 102250 | |
sipa.codpersvinculados | 3538 | |
sipa.codpersvinculados | 102379 | |
sipa.index | WOS | |
sipa.index | Scopus | |
sipa.trazabilidad | Carga SIPA;09-01-2024 |
Files
Original bundle
1 - 1 of 1
Loading...
- Name:
- Effects of Japanese herbal medicine inchin-ko-to on endotoxin-induced cholestasis in the rat.pdf
- Size:
- 106.2 KB
- Format:
- Adobe Portable Document Format
- Description: