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. Author manuscript; available in PMC: 2014 Dec 1.
Published in final edited form as: J Pharm Sci. 2013 Oct 15;102(12):4444–4454. doi: 10.1002/jps.23753

Figure 2. BME inhibits the interaction of DOX with multidrug resistance proteins altering its bioavailability within the cancer cells.

Figure 2

(A) Time dependent uptake of doxorubicin. The uptake is linear for first 30 min of exposure in HT-29 cells. (B) Both pre-incubation and co-incubation of BME increases the uptake of DOX at 37°C. The white bars represent the doxorubicin uptake at 50 µM for 30 min in cells pretreated with different concentrations of BME for 48 h. The black bars represent doxorubicin uptake at 50 µM for 30 min when incubated in combination with different concentrations of BME. All these studies were carried out at 37°C. *p<0.05. (C) BME treatment of DOX affects active transport of DOX as there is no difference in the uptake of DOX at 4°C. The white bars represent the doxorubicin uptake at 50 µM for 30 min in cells pretreated with different concentrations of BME for 48 h. The black bars represent the doxorubicin uptake at 50µM for 30 min in combination with different concentrations of BME. All these studies were carried out at 4°C. (D) Highest MDR gene expression is achieved 48 h post seeding which then normalizes by 72 h. *p<0.05. (E & F) BME pretreatment reduces the expression of MDR proteins both in a concentration dependent (panel E) and time dependent manner (panel F). In panel E, cells were treated with different concentrations of BME for 48 h, while in panel F, they were treated with 25 µg/mL BME for different time points. *p<0.05.