Fig 1: Protein levels of apoptosis biomarker. The level of Caspase-3 (A), p53 (B), Bax (C), and Bcl-2 (D) in HepG-2, MCF-7, Bj-1, and MCF-12F treated with or without the IC50 of MP, MP/NabM, and MP/IHM. MP: milk proteins concentrate; MP/NabM: milk proteins/Nabeq mucilage complex; MP/IHM: milk proteins/Isabgol husk mucilage complex. Data are average of triplicates. Measurements with different letters (a, b, c and d) are significantly different (p < 0.05).
Fig 2: miR-421 mimics reverse the effects of Rian-plasmid on MLE-12 cell viability and apoptosis. Following stimulation (hyperoxia induction) and transfection, cells were divided into six groups: Control, hyperoxia, hyperoxia + control-plasmid, hyperoxia + Rian-plasmid, hyperoxia + Rian-plasmid + mimics control, or hyperoxia + Rian-plasmid + miR-421 mimics groups. Reverse transcription-quantitative PCR of (A) Rian and (B) miR-421 expression in different groups. (C) Cell viability was evaluated with an MTT assay. (D) Apoptotic cells were determined using flow cytometry. (E) Quantitative analysis of apoptotic cells from D. (F) Determination of caspase-3 activity in different groups. **P<0.01 vs. Control; ##P<0.01 vs. hyperoxia + control-plasmid group; &&P<0.01 vs. hyperoxia + Rian-plasmid + mimics control group. miR, microRNA; Rian, RNA imprinted and accumulated in nucleus.
Fig 3: Effect of KYP-2047 on transforming growth factor-ß (TGF-ß) and caspase-3 expression in U-87 cells. Immunofluorescence assay performed on U-87 cells revealed a marked expression of TGF-ß in the control group (A), while the treatment with KYP-2047 at the concentrations of 50 µM and 100 µM reduced significantly TGF-ß expression (B,C). Additionally, immunofluorescence staining showed an increase of caspase-3 levels in the groups treated with KYP-2047 at the concentrations of 50 µM and 100 µM (F,G) compared to control group (E). Data are representative of at least three independent experiments. (D) ### p < 0.001 vs. CTR; (H) ## p < 0.01 vs. CTR; ### p < 0.001 vs. CTR.
Fig 4: Changes in the transcript expression levels of the selected inflammation-associated genes (COX2 and NFκB), proto-oncogene (CTNNB1), autophagy-associated gene (CTSB), and apoptosis-associated genes (BCL2, CASP3, CASP7, CASP8, and CASP9). SKOV-3 cells were cultured with 0.1% (v/v) dimethyl sulfoxide (DMSO) alone (control) or DMSO containing α-mangostin (7.309 μM), apigenin (18.502 μM), or doxorubicin (0.431 μM) for 24 hr. Data are shown as the mean ± 1SD, derived from three independent repeats. * and ** represent a significant difference between the control and treated cells in each group at p < 0.05 or p<0.01, respectively.
Fig 5: Relative caspase activity in doxorubicin-, α-mangostin-, and apigenin-treated SKOV-3 cells. Cells were treated with 0.1% (v/v) dimethyl sulfoxide (DMSO) alone (control) or DMSO containing α-mangostin (7.309 μM), apigenin (18.502 μM), or doxorubicin (0.431 μM) for 12 and 24 hr and then assayed for (A) caspase-8, (B) caspase-9, and (C) caspase-3 activity. Data are shown as the mean ± 1SD, derived from three replications, where * and ** represent a significant difference between the control and treated cells at p < 0.05 and p < 0.01, respectively.
Supplier Page from Abcam for Caspase-3 Assay Kit (Colorimetric)