Liver, Pancreas, and Biliary TractEffects of Ursodeoxycholic and Cholic Acid Feeding on Hepatocellular Transporter Expression in Mouse Liver
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Drug Transporters: Efflux
2022, Comprehensive PharmacologyTianJiu therapy for α-naphthyl isothiocyanate-induced intrahepatic cholestasis in rats treated with fresh Ranunculus sceleratus L.
2020, Journal of EthnopharmacologyAnticholestatic mechanisms of ursodeoxycholic acid in lipopolysaccharide-induced cholestasis
2019, Biochemical PharmacologyCitation Excerpt :Similarly to Bsep, Mrp2 gene transcription was enhanced by UDCA in LPS cholestatic rats (see Table 6); this may reflect, again, the capability of UDCA to counteract cytokine-mediated effects on Mrp2 transcription mechanisms, which is also JNK-dependent in nature [63,65]. In addition, the well characterized inductive effect that UDCA has per se on Mrp2 expression [60] may be another contributing factor. Surprisingly, an enhanced Mrp2 mRNA levels in the co-treated group did not lead to an improved expression of Mrp2 either at the protein level (see Table 4) or at a functional levels, as evaluated by assessing the biliary excretion of its exogenous substrate, BSP (see Fig. 2).
Increased Expression of Renal Drug Transporters in a Mouse Model of Familial Alzheimer's Disease
2019, Journal of Pharmaceutical SciencesCitation Excerpt :It is possible that elevated plasma Aβ in APP/PS1 mice27 may also alter renal transporter and metabolizing enzymes expression, which has not yet been studied. It is also very likely that given that plasma levels of bile acids and inflammatory mediators are also modified in AD, and they have been reported to affect the expression of peripheral transporters,11,26 the modified expression of the transporters observed could be a result of not only Aβ but also bile acids and inflammatory mediators. In summary, these studies have demonstrated that the renal expression of key drug transporters Mrp2, Oct2, and Oat3 is modestly, but significantly, increased in a mouse model of familial AD.
Animal models to study bile acid metabolism
2019, Biochimica et Biophysica Acta - Molecular Basis of DiseaseCitation Excerpt :In wild type mice, expression of Cyp7a1, Cyp7b1, and the sinusoidal membrane bile acid uptake transporters Ntcp and Oatp1a1 are down-regulated by CA feeding [49,252], whereas expression of the canalicular membrane transporters Bsep, Mrp2, and Mdr1a/b is up-regulated [252]. Liver morphological changes induced by CA feeding includes disseminated hepatocyte necrosis, increased cell size, increased number of mitotic figures, and dilation of interlobular bile ducts [252]. Feeding CA (typically ~0.5%) to mice with genetic defects in bile acid biosynthetic enzymes or transporters is typically used to unmask susceptibilities to liver injury.