rifampin has been researched along with verlukast* in 3 studies
3 other study(ies) available for rifampin and verlukast
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ABC transporters affect the elimination and toxicity of CdTe quantum dots in liver and kidney cells.
This paper aimed to investigate the role of adenosine triphosphate-binding cassette (ABC) transporters on the efflux and the toxicity of nanoparticles in liver and kidney cells. In this study, we synthesized CdTe quantum dots (QDs) that were monodispersed and emitted green fluorescence (maximum peak at 530nm). Such QDs tended to accumulate in human hepatocellular carcinoma cells (HepG2), human kidney cells 2 (HK-2), and Madin-Darby canine kidney (MDCK) cells, and cause significant toxicity in all the three cell lines. Using specific inhibitors and inducers of P-glycoprotein (Pgp) and multidrug resistance associated proteins (Mrps), the cellular accumulation and subsequent toxicity of QDs in HepG2 and HK-2 cells were significantly affected, while only slight changes appeared in MDCK cells, corresponding well with the functional expressions of ABC transporters in cells. Moreover, treatment of QDs caused concentration- and time- dependent induction of ABC transporters in HepG2 and HK-2 cells, but such phenomenon was barely found in MDCK cells. Furthermore, the effects of CdTe QDs on ABC transporters were found to be greater than those of CdCl2 at equivalent concentrations of cadmium, indicating that the effects of QDs should be a combination of free Cd(2+) and specific properties of QDs. Overall, these results indicated a strong dependence between the functional expressions of ABC transporters and the efflux of QDs, which could be an important reason for the modulation of QDs toxicity by ABC transporters. Topics: Animals; ATP-Binding Cassette Transporters; Cadmium Compounds; Cell Line; Cell Survival; Cyclosporine; Dogs; Hep G2 Cells; Humans; Kidney; Liver; Madin Darby Canine Kidney Cells; Oligopeptides; Probenecid; Propionates; Quantum Dots; Quinolines; Rifampin; RNA, Messenger; Tellurium | 2016 |
Quantitative time-lapse imaging-based analysis of drug-drug interaction mediated by hepatobiliary transporter, multidrug resistance-associated protein 2, in sandwich-cultured rat hepatocytes.
There is increasing interest in developing efficient screening platforms to predict drug-induced liver injury. Therefore, we explored a microscope-based analysis to quantitatively evaluate interaction of drugs with multidrug resistance-associated protein 2 (MRP2), essential for hepatic excretion of drugs in sandwich-cultured rat hepatocytes (SCRHs), using 5 (and 6)-carboxy-2',7'-dichlorofluorescein (CDF) diacetate, which is intracellularly hydrolyzed to the fluorescent substrate CDF. Drug-MRP2 interactions were evaluated by measuring the fluorescence change in bile canaliculi in SCRHs in the presence or absence of MRP2 inhibitors using quantitative time-lapse imaging (QTLI) analysis. Fluorescence was negligible in SCHs from rat (r) Mrp2-deficient Eisai hyperbilirubinemic rat, suggesting that Mrp2 is primarily responsible for CDF accumulation. According to QTLI, rifampicin, cyclosporine, and 3-[[3-[2-(7-chloroquinolin-2-yl)vinyl]phenyl]-(2-dimethylcarbamoylethylsulfanyl)methylsulfanyl] propionic acid (MK-571) attenuated CDF accumulation in a concentration-dependent manner, with IC₅₀ values (IC₅₀, QTLI)) of 3.02, 1.63, and 2.87 μM, respectively. The ratios of IC₅₀ values obtained from the biliary excretion index over the IC(₅₀, QTLI) were 1.34, 1.94, and 1.94, but ratios over IC₅₀ values in CDF uptake by Mrp2-expressing membrane vesicles varied more: 6.69, 3.07, and 2.43 for rifampicin, cyclosporine, and MK-571, respectively. When the IC(₅₀, QTLI) of rifampicin was corrected for the hepatocyte/medium distribution ratio, the relative ratio of IC(₅₀, VES)/IC(₅₀, QTLI) was reduced to 2.25 from 6.69 (20.2/3.02) and was close to the ratio for MK-571 (2.43, 6.96/2.87), which is thought to cross the plasma membrane by passive diffusion. Our results indicate that QTLI is a suitable method to evaluate drug-MRP2 interaction at the bile canalicular membrane, when the hepatocyte/medium distribution ratio in SCRHs is taken into account. Topics: Animals; ATP-Binding Cassette Transporters; Bile Canaliculi; Cell Culture Techniques; Cell Membrane; Cells, Cultured; Cyclosporine; Drug Interactions; Fluoresceins; Fluorescent Dyes; Hepatocytes; Hyperbilirubinemia; Male; Microscopy, Fluorescence; Molecular Imaging; Pharmaceutical Preparations; Propionates; Quinolines; Rats; Rats, Sprague-Dawley; Rats, Wistar; Rifampin | 2011 |
Up-regulation of P-glycoprotein by HIV protease inhibitors in a human brain microvessel endothelial cell line.
A major concern regarding the chronic administration of antiretroviral drugs is the potential for induction of drug efflux transporter expression (i.e., P-glycoprotein, P-gp) at tissue sites that can significantly affect drug distribution and treatment efficacy. Previous data have shown that the inductive effect of human immunodeficiency virus protease inhibitors (PIs) is mediated through the human orphan nuclear receptor, steroid xenobiotic receptor (SXR or hPXR). The objectives of this study were to investigate transport and inductive properties on efflux drug transporters of two PIs, atazanavir and ritonavir, at the blood-brain barrier by using a human brain microvessel endothelial cell line, hCMEC/D3. Transport properties of PIs by the drug efflux transporters P-gp and multidrug resistance protein 1 (MRP1) were assessed by measuring the cellular uptake of (3)H-atazanavir or (3)H-ritonavir in P-gp and MRP1 overexpressing cells as well as hCMEC/D3. Whereas the P-gp inhibitor, PSC833, increased atazanavir and ritonavir accumulation in hCMEC/D3 cells by 2-fold, the MRP inhibitor MK571 had no effect. P-gp, MRP1, and hPXR expression and localization were examined by Western blot analysis and immunogold cytochemistry at the electron microscope level. Treatment of hCMEC/D3 cells for 72 hr with rifampin or SR12813 (two well-established hPXR ligands) or PIs (atazanavir or ritonavir) resulted in an increase in P-gp expression by 1.8-, 6-, and 2-fold, respectively, with no effect observed for MRP1 expression. In hCMEC/D3 cells, cellular accumulation of these PIs appears to be primarily limited by P-gp efflux activity. Long-term exposure of atazanavir or ritonavir to brain microvessel endothelium may result in further limitations in brain drug permeability as a result of the up-regulation of P-gp expression and function. Topics: Atazanavir Sulfate; ATP Binding Cassette Transporter, Subfamily B, Member 1; Blood-Brain Barrier; Brain; Cell Line; Cyclosporins; Diphosphonates; Endothelium, Vascular; HIV Protease Inhibitors; Humans; Microvessels; Oligopeptides; Propionates; Pyridines; Quinolines; Rifampin; Ritonavir; Tritium; Up-Regulation | 2009 |