scholarly journals Impact of chrysosplenetin, per se or in combination with artemisinin, on breast cancer resistance protein (Bcrp)/ABCG2 mRNA expression levels in mice small intestine

2017 ◽  
Vol 27 (6) ◽  
pp. 776-779
Author(s):  
Wei Ma ◽  
Yuanyuan Zhang ◽  
Yanli Zhang ◽  
Chenxu Zhang ◽  
Jianhuan Wang ◽  
...  
2011 ◽  
Vol 39 (11) ◽  
pp. 2148-2154 ◽  
Author(s):  
Takuya Shimizu ◽  
Tomoko Sugiura ◽  
Tomohiko Wakayama ◽  
Ai Kijima ◽  
Noritaka Nakamichi ◽  
...  

2009 ◽  
Vol 12 (2) ◽  
pp. 150 ◽  
Author(s):  
Atsushi Kawase ◽  
Yukako Matsumoto ◽  
Motoshi Hadano ◽  
Yui Ishii ◽  
Masahiro Iwaki

PURPOSE: The activities of breast cancer resistance protein (Bcrp/ABCG2) as well as P-glycoprotein (P-gp) and drug-metabolizing enzymes can be inhibited by several flavonoids or drugs in rats. However, the species, gender and regional differences of effects of flavonoids on Bcrp/ABCG2 in rats and mice remain unclear, although Bcrp, like P-gp, is also important in controlling drug absorption and disposition. METHODS: We used chrysin as a model flavonoid because it possesses anti-inflammatory and antioxidative properties and is used as a dietary supplement. We examined the pharmacokinetics of nitrofurantoin, a specific Bcrp substrate, in rats and mice treated with chrysin. Bcrp mRNA levels were measured in liver, kidney, duodenum, jejunum and ileum in rats and mice. RESULTS: Plasma concentrations of nitrofurantoin were increased in rats, but not mice, treated with oral chrysin, compared with untreated controls. Intraperitoneal injection of chrysin into rats or mice had little effect on the elimination of nitrofurantoin, compared with untreated animals. CONCLUSIONS: These results suggest that chrysin-nitrofurantoin interactions occur in the small intestine in rats, but not in mice, possibly due to the higher levels of Bcrp expression in the small intestine in rats, compared with those in mice.


Author(s):  
Erlia Anggrainy Sianipar ◽  
Melva Louisa ◽  
Septelia Inawati Wanandi

The decreasing of sensitivity or resistance to tamoxifen occured after long-term treatment in breast cancer. One of the major factor in tamoxifen resistance is over expression of efflux transporter P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP). Curcumin has known as inhibitor of P-gp and BCRP. The addition of curcumin to the tamoxifen resistant cells is expected to increase the sensitivity of breast cancer cells to tamoxifen. This study aim to know the effect of curcumin in increasing the cell sensitivity to tamoxifen through inhibition of P-gp and BCRP transporter efflux. MCF-7 breast cancer cell line was induced with tamoxifen 1 µM for 10 passage (MCF-7(T)), then cell viability and mRNA expression of P-gp and BCRP were analyzed. To the MCF-7(T) cells, curcumin was given at of 5/10/20 µM with or without tamoxifen for 5 days and cell viability and mRNA expression of P-gp and BCRP were analyzed on day 5th.  As positive control, verapamil 50 µM was used as P-gp inhibitor, ritonavir 15 µM and nelfinavir 15 µM were used as BCRP inhibitor.  The results showed that MCF-7(T) cells sensitivity to tamoxifen decreased with 11.8 times, the cell viability increased 10.82 fold and mRNA expression of P-gp and BCRP increased 4.04 fold. Then after administration of curcumin with or without tamoxifen for 5 days, the cell viability and the mRNA expression of P-gp and BCRP decreased. As conclusion, curcumin increased the sensitivity of MCF-7(T) to tamoxifen characterized by the decreasing of cell viability and mRNA expression of P-gp and BCRP. However, the administration of combination of curcumin with tamoxifen was more potent than just curcumin. The increased sensitivity was estimated at least partly through the inhibition of P-gp and BCRP mRNA expression by curcumin


2005 ◽  
Vol 70 (5) ◽  
pp. 695-699 ◽  
Author(s):  
Heike Gutmann ◽  
Petr Hruz ◽  
Christian Zimmermann ◽  
Christoph Beglinger ◽  
Juergen Drewe

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4367-4367
Author(s):  
A. Ugur Ural ◽  
Ozlem Darcansoy Iseri ◽  
Pelin Kaya Mutlu ◽  
Meltem Demirel Kars ◽  
Ferit Avcu ◽  
...  

Abstract One of the major problems in the treatment of leukemia is the development of drug resistance to chemotherapeutic agents, which is already present at diagnosis or after chemotherapy as a minimal residual disease. The resistance may be originated from genetic or epigenetic mutations during prior growth of the leukemic clone. In this study, the expressions of three multidrug resistance (MDR) genes were investigated. Expression levels of multidrug resistance resistance gene 1 (MDR1), breast cancer resistance protein (BCRP) gene, and lung resistance protein (LRP) gene expression levels were determined in peripheral blood samples from 16 cases of chronic lymphocytic leukemia (CLL) and from 23 cases of chronic myelogeneous leukemia (CML) using RT-PCR. The expression of each of these genes was then expressed as a ratio in relation to β2-microglobulin gene expression in densitometric measurements. MDR1, BCRP and LRP expression levels was detected in 56,3%, 18,8% and 50% of CLL patients, respectively, with no difference for stage or response to the treatment. Four out of 16 (25%) CLL patients expressed none of these genes. The other 25% CLL patients expressed all of these genes. MDR1, BCRP and LRP expression was detected in 47,8%, 39,1% and 30,4% of CML patients, respectively, with no difference for progression or response to imatinib mesylate. Eight out of 23 (34,8%) CML patients expressed none of these genes. Four out of 23 (17,4%) CML patients expressed all of these genes, and two out of whom rapidly progressed to acute leukemia and unresponsive to the treatment. In conclusion, MDR and LRP overexpression seems to be a frequent event in CLL and CML patients; however no conclusion can be drawn on their prognostic role and response to the treatment.


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