Journal: Frontiers in Pharmacology

Article Title: Doxorubicin resistance in breast cancer is mediated via the activation of FABP5/PPARγ and CaMKII signaling pathway

doi: 10.3389/fphar.2023.1150861

Figure Lengend Snippet: Validation of MCF-7/ADR cell drug resistance qualities. (A) MCF-7 cells vary morphologically from MCF-7/ADR cells, MCF-7 cells are spherical shape spheres whereas MCF-7/ADR cells are polyhedral. (B) CCK-8 assay was used to determine the IC 50 values of MCF-7 and MCF-7/ADR cells following treatment of Dox at various doses for 48 h. (C) Analysis of the expression of two resistant proteins (MRP1, P-GP) in MCF-7/ADR and MCF-7 cells using WB( n = 3). (D) After 24 h of treatment with 5 μM Dox, drug accumulation in MCF-7 cells and MCF-7/ADR cells was observed via confocal microscopy. Red fluorescence is the spontaneous color of Dox, blue is the color of the nucleus stained by Hoechst 33,342 and fuchsia is the merge, the intracellular Dox accumulation to be observed, and statistical fluorescence by ImageJ (n = 6), scale 0–75 μm *** p < 0.001 vs. MCF-7 cells.

Article Snippet: For membrane labeling, the antibodies include P-GP (1:3,000, HUABIO, China), Multidrug resistance-associated protein (MRP1) (1:3,000, HUABIO, China), Microtubule Associated Protein 1 Light Chain 3 Beta (MAP1LC3B) (1:1,000, ABclonal, China), P62 (1:6,000, MBL, United States), Peroxisome proliferator-activated receptor γ (PPARγ, 1:1,000,proteintech, United States), FABP5 (1:500, proteintech, United States), CaMKII (1:500, ABclonal, China), p-CaMKII (1:500, ABclonal, China), and GAPDH (1:10,000, proteintech, United States) ( ).

Techniques: CCK-8 Assay, Expressing, Confocal Microscopy, Fluorescence, Staining

Journal: PLoS ONE

Article Title: Gene Silencing of FANCF Potentiates the Sensitivity to Mitoxantrone through Activation of JNK and p38 Signal Pathways in Breast Cancer Cells

doi: 10.1371/journal.pone.0044254

Figure Lengend Snippet: (A) T-47D and MCF-7 cells were transfected with FANCF shRNA or control shRNA for 48 h, and then treated with 10 uM MX for 24 h. The cell viability was determined by the MTT assay. The percentage of viable cells was determined by the ratio of viable cells treated with MX to that with no MX treatment. (B) Median fluorescene intensity was measured indicating the relative amount of MX accumulation. (C) Quantitative analysis of the fold increase of fluorescence intensity in FANCF- silenced MCF-7 and T-47D cells compared with the controls. P values, # P <0.05. (D) MRP/LRP/P-gp/ BCRP protein expression was detected by western blot assay. (E) Densitometric analysis was done for BCRP expression. P values, # P <0.05 versus transfected with FANCF shRNA and MX in MCF-7 cells,★ P <0.05 versus transfected with FANCF shRNA and MX in T-47D cells.

Article Snippet: Antibodies against p53, phospho-p53, breast cancer resistance protein (BCRP), multidrug resistance-associated protein (MRP), lung resistance protein (LRP) and P-glycoprotein (P-gp) were from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

Techniques: Transfection, shRNA, MTT Assay, Fluorescence, Expressing, Western Blot

Journal: Frontiers in Pharmacology

Article Title: Idiosyncratic liver injury induced by bolus combination treatment with emodin and 2,3,5,4′-tetrahydroxystilbene-2- O - β -D-glucopyranoside in rats

doi: 10.3389/fphar.2022.1017741

Figure Lengend Snippet: Plasma levels of the inflammatory cytokines after oral administrations of vehicle control, TSG, emodin and their combination to normal rats (Normal) and LPS-mediated inflammatory stress model rats (LPS), * p < 0.05 by two-way ANOVA followed by the Tukey post hoc test, ND, not detectable (A) ; protein expression of bile acid synthesis enzymes (CYP7A1, CYP27A1), efflux transporters (BSEP, MRP2, MRP3, MRP4) and apoptosis-related proteins (BAX, BCL-2, Cleaved CASPASE-9, Cleaved CASPASE-3) in the liver after oral administration with vehicle control to normal or LPS-mediated inflammatory stress model rats, * p < 0.05, ** p < 0.01 by Student t-test (B) . Data are represented as mean ± SD ( n = 6).

Article Snippet: Primary antibodies for cholesterol 7α-hydroxylase (CYP7A1), sterol 27-hydroxylase (CYP27A1), bile salt export pump (BSEP), BAX, BCL-2 were supplied by Santa Cruz Biotechnology (Dallas, TX, United States), multidrug resistance-associated proteins 2 (MRP2) and MRP3 were from Thermo Fisher Scientific (Cleveland, OH, United States), and that of Cleaved CASPASE-3, Cleaved CASPASE-9, MRP4, β-ACTIN and all secondary antibodies were purchased from Abcam (Cambridge, MA, United States).

Techniques: Clinical Proteomics, Control, Expressing

Journal: Frontiers in Pharmacology

Article Title: Idiosyncratic liver injury induced by bolus combination treatment with emodin and 2,3,5,4′-tetrahydroxystilbene-2- O - β -D-glucopyranoside in rats

doi: 10.3389/fphar.2022.1017741

Figure Lengend Snippet: Protein expression of bile acid synthesis enzymes (CYP7A1 and CYP27A1), bile acid efflux transporters (BSEP, MRP2, MRP3, and MRP4) and apoptosis-related proteins (BAX, BCL-2, Cleaved CASPASE-3, and Cleaved CASPASE-9) in the liver after oral administration with emodin, TSG or their combination to normal rats (A,C) or LPS-mediated inflammatory stress model rats (B,D) . The data are expressed as mean ± SD ( n = 6). * p < 0.05, ** p < 0.01, *** p < 0.001 by two-way ANOVA followed by the Tukey post hoc test.

Article Snippet: Primary antibodies for cholesterol 7α-hydroxylase (CYP7A1), sterol 27-hydroxylase (CYP27A1), bile salt export pump (BSEP), BAX, BCL-2 were supplied by Santa Cruz Biotechnology (Dallas, TX, United States), multidrug resistance-associated proteins 2 (MRP2) and MRP3 were from Thermo Fisher Scientific (Cleveland, OH, United States), and that of Cleaved CASPASE-3, Cleaved CASPASE-9, MRP4, β-ACTIN and all secondary antibodies were purchased from Abcam (Cambridge, MA, United States).

Techniques: Expressing