Journal: PLoS ONE

Article Title: Regulation of Multidrug Resistance Proteins by Genistein in a Hepatocarcinoma Cell Line: Impact on Sorafenib Cytotoxicity

doi: 10.1371/journal.pone.0119502

Figure Lengend Snippet: Calcein accumulation is directly associated to accumulation of its non fluorescent precursor calcein-AM (P-gp substrate) and was quantified by flow cytometry in control (C) and GNT treated cells (1.0 and 10 μM, 48 h) in the absence (- PSC) or presence (+ PSC) of the P-gp specific inhibitor PSC833 (10 μM). Data (mean ± S.D., n = 3) are presented as fold change of the calcein accumulation in C—PSC, considered as 1. a: different from C—PSC, b: different from GNT 1.0 μM—PSC; c: different from GNT 10—PSC. p<0.05.

Article Snippet: PSC833 and calcein-AM were from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

Techniques: Flow Cytometry, Control

Journal: PLoS ONE

Article Title: Regulation of Multidrug Resistance Proteins by Genistein in a Hepatocarcinoma Cell Line: Impact on Sorafenib Cytotoxicity

doi: 10.1371/journal.pone.0119502

Figure Lengend Snippet: Effect of GNT on sorafenib-induced cytotoxicity.

Article Snippet: PSC833 and calcein-AM were from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

Techniques: Control

Journal: Neuropharmacology

Article Title: Differences in amyloid-β clearance across mouse and human blood-brain barrier models: Kinetic analysis and mechanistic modeling

doi: 10.1016/j.neuropharm.2014.01.023

Figure Lengend Snippet: Total brain clearance (BCITotal(%)) of 125I-Aβ40 in control (CNTRL), with P-gp inhibitor valspodar (VALSP) or LRP1 inhibitor RAP (A), BBB clearance (BCIBBB(%)) of 125I-Aβ40 in control and inhibitor groups (B), clearance of 125I-Aβ40 by brain degradation (BCIDegradation(%)) in control and inhibitor groups (C). Data represent mean±SEM for n=4; * P<0.05, ** P<0.01 and *** P<0.001. NS is not significant.

Article Snippet: To characterize role of P-gp and LRP1, 0.5 μl of ECF containing valspodar (40 μM; XenoTech, KS), a well-established P-gp inhibitor, or RAP (1 μM; Oxford Biomedical Research, MI), an LRP1 inhibitor, were intracerebrally administered 5 min prior to 125 I-Aβ 40 injection.

Techniques: Control

Journal: Neuropharmacology

Article Title: Differences in amyloid-β clearance across mouse and human blood-brain barrier models: Kinetic analysis and mechanistic modeling

doi: 10.1016/j.neuropharm.2014.01.023

Figure Lengend Snippet: A) In vitro uptake of intact 125I-Aβ40 by bEnd3 and hCMEC/D3 cells. Cellular level of intact 125I-Aβ40 is expressed in fmole/mg protein following cells treatment with 0.1 nM 125I-Aβ40 without (control; CNTRL) and with RAGE (RAGE-IgG), or P-gp (valspodar; VALSP), or LRP1 (RAP) inhibitors for 15 min and 12 h in bEnd3 and hCMEC/D3, respectively. B) Percent of degraded 125I-Aβ40 in the media of bEnd3 and hCMEC/D3 cells following treatment with 0.1 nM of 125I-Aβ40, with or without inhibitor. Data represent mean±SEM from three independent experiments; *P<0.05, **P< 0.01 and *** P<0.001.

Article Snippet: To characterize role of P-gp and LRP1, 0.5 μl of ECF containing valspodar (40 μM; XenoTech, KS), a well-established P-gp inhibitor, or RAP (1 μM; Oxford Biomedical Research, MI), an LRP1 inhibitor, were intracerebrally administered 5 min prior to 125 I-Aβ 40 injection.

Techniques: In Vitro, Control