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Elabscience Biotechnology annexin v fitc pi apoptosis detection kit

Roles of the CD39/CD73 axis on DUB's multidirectional protection effects in Dex-treated primary BMSCs. ( A ) ELISA for ROS clearance-related enzyme T-SOD and ROS damage biomarkers 8-OHdG, AOPP, and MDA in primary BMSCs of different groups. ( B ) Western blot and quantification for the expression of ROS clearance-related proteins in primary BMSCs of different groups. ( C ) Representative images and quantitative analysis of immunofluorescence staining for MitoSox (red) in primary BMSCs of different groups, and nuclei were stained with Hoechst (blue). ( D ) Western blot and quantification for the expression of <t>apoptosis-related</t> proteins in primary BMSCs of different groups. ( E ) Cellular apoptosis detection in primary BMSCs of different groups by <t>Annexin</t> V-FITC and PI dual-staining assessment via flow cytometry. The proportion of cells in each quadrant was indicated in the plot. ( F ) Tunel (red) staining and quantification of apoptotic cells in primary BMSCs of different groups, and nuclei were stained with DAPI (blue). ( G ) Representative images and quantitative analysis of Alizarin Red S staining for mineralization in primary BMSCs of different groups under osteogenic conditions. ( H ) Western blot and quantification for the expression of osteogenesis-related proteins in primary BMSCs of different groups. n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 50 μm (C), 25 μm (F), and 200 μm (G).

Annexin V Fitc Pi Apoptosis Detection Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 98/100, based on 909 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Screening of a quinonoid compounds library identifies decylubiquinone as an antioxidant and anti-apoptotic agent against glucocorticoid-induced osteoporosis via CD39/CD73/adenosine axis"

Article Title: Screening of a quinonoid compounds library identifies decylubiquinone as an antioxidant and anti-apoptotic agent against glucocorticoid-induced osteoporosis via CD39/CD73/adenosine axis

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.03.062

Figure Legend Snippet: Roles of the CD39/CD73 axis on DUB's multidirectional protection effects in Dex-treated primary BMSCs. ( A ) ELISA for ROS clearance-related enzyme T-SOD and ROS damage biomarkers 8-OHdG, AOPP, and MDA in primary BMSCs of different groups. ( B ) Western blot and quantification for the expression of ROS clearance-related proteins in primary BMSCs of different groups. ( C ) Representative images and quantitative analysis of immunofluorescence staining for MitoSox (red) in primary BMSCs of different groups, and nuclei were stained with Hoechst (blue). ( D ) Western blot and quantification for the expression of apoptosis-related proteins in primary BMSCs of different groups. ( E ) Cellular apoptosis detection in primary BMSCs of different groups by Annexin V-FITC and PI dual-staining assessment via flow cytometry. The proportion of cells in each quadrant was indicated in the plot. ( F ) Tunel (red) staining and quantification of apoptotic cells in primary BMSCs of different groups, and nuclei were stained with DAPI (blue). ( G ) Representative images and quantitative analysis of Alizarin Red S staining for mineralization in primary BMSCs of different groups under osteogenic conditions. ( H ) Western blot and quantification for the expression of osteogenesis-related proteins in primary BMSCs of different groups. n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 50 μm (C), 25 μm (F), and 200 μm (G).

Techniques Used: Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Immunofluorescence, Staining, Flow Cytometry, TUNEL Assay, In Vitro

The effect of ADO supplements on primary BMSCs. ( A ) MTT assay for the proliferation of BMSCs treated with different doses of ADO for 2 days and 10 days under osteogenic induction conditions with or without 10 μM Dex. ( B-C ) Representative images and quantitative analysis of mineralized nodule areas by Alizarin Red S staining in primary BMSCs treated with gradient doses of ADO under osteogenic induction with or without 10 μM Dex. ( D ) Western blot and quantification for the expression of osteogenesis-related proteins in primary BMSCs of different groups. ( E ) ELISA for ROS clearance-related enzyme T-SOD and ROS damage biomarkers 8-OHdG, AOPP, and MDA in primary BMSCs of different groups. ( F ) Western blot and quantification for the expression of ROS clearance-related proteins in primary BMSCs of different groups. ( G ) Representative images and quantitative analysis of immunofluorescence staining for MitoSox (red) in primary BMSCs of different groups, and nuclei were stained with Hoechst (blue). ( H ) Western blot and quantification for the expression of apoptosis-related proteins in primary BMSCs of different groups. ( I ) Cellular apoptosis detection in primary BMSCs of different groups by Annexin V-FITC and PI dual-staining assessment via flow cytometry. The proportion of cells in each quadrant was indicated in the plot. ( J ) Tunel (red) staining and quantification of apoptotic cells in primary BMSCs of different groups, and nuclei were stained with DAPI (blue). n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 200 μm (B), 50 μm (G), and 25 μm (J).

Figure Legend Snippet: The effect of ADO supplements on primary BMSCs. ( A ) MTT assay for the proliferation of BMSCs treated with different doses of ADO for 2 days and 10 days under osteogenic induction conditions with or without 10 μM Dex. ( B-C ) Representative images and quantitative analysis of mineralized nodule areas by Alizarin Red S staining in primary BMSCs treated with gradient doses of ADO under osteogenic induction with or without 10 μM Dex. ( D ) Western blot and quantification for the expression of osteogenesis-related proteins in primary BMSCs of different groups. ( E ) ELISA for ROS clearance-related enzyme T-SOD and ROS damage biomarkers 8-OHdG, AOPP, and MDA in primary BMSCs of different groups. ( F ) Western blot and quantification for the expression of ROS clearance-related proteins in primary BMSCs of different groups. ( G ) Representative images and quantitative analysis of immunofluorescence staining for MitoSox (red) in primary BMSCs of different groups, and nuclei were stained with Hoechst (blue). ( H ) Western blot and quantification for the expression of apoptosis-related proteins in primary BMSCs of different groups. ( I ) Cellular apoptosis detection in primary BMSCs of different groups by Annexin V-FITC and PI dual-staining assessment via flow cytometry. The proportion of cells in each quadrant was indicated in the plot. ( J ) Tunel (red) staining and quantification of apoptotic cells in primary BMSCs of different groups, and nuclei were stained with DAPI (blue). n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 200 μm (B), 50 μm (G), and 25 μm (J).

Techniques Used: MTT Assay, Staining, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Flow Cytometry, TUNEL Assay, In Vitro

Summary of the study. The schematic diagram illustrates that DUB alleviates GIOP by suppressing oxidative stress and apoptosis via the CD39/CD73/ADO axis and promotes osteogenesis via ADO/A 2b R-mediated activation of the PKA/CREB pathway. The schematic diagram was created by using BioRender.com.

Figure Legend Snippet: Summary of the study. The schematic diagram illustrates that DUB alleviates GIOP by suppressing oxidative stress and apoptosis via the CD39/CD73/ADO axis and promotes osteogenesis via ADO/A 2b R-mediated activation of the PKA/CREB pathway. The schematic diagram was created by using BioRender.com.

Techniques Used: Activation Assay

Image Search Results

Screening of genes in EC. (A) The Venn diagram shows the intersection between the DEGs in EC and normal esophageal tissues and the genes related to apoptosis, proliferation, and glycolysis. (B-D) The Lasso regression, SVM, and RF algorithms were used to further screen the 11 genes and identify key signature genes. (E) The Venn diagram shows the key genes identified by the Lasso regression, SVM, and RF algorithms.

Journal: Regenerative Therapy

Article Title: WTAP stabilizes MMP12 expression to promote the malignant phenotypes of esophageal cancer cells

doi: 10.1016/j.reth.2026.101101

Figure Lengend Snippet: Screening of genes in EC. (A) The Venn diagram shows the intersection between the DEGs in EC and normal esophageal tissues and the genes related to apoptosis, proliferation, and glycolysis. (B-D) The Lasso regression, SVM, and RF algorithms were used to further screen the 11 genes and identify key signature genes. (E) The Venn diagram shows the key genes identified by the Lasso regression, SVM, and RF algorithms.

Article Snippet: Apoptosis was evaluated using a Double Staining Apoptosis Kit (Vazyme Biotech, Nanjing, China) following the protocol for Annexin V-FITC and propidium iodide dual staining.

Techniques:

MMP12 knockdown inhibited the migration, invasion, proliferation, and glucose metabolism and induced cell apoptosis. KYSE150 cells were transfected with si-MMP12 or si-NC. (A and B) Cell migration and invasion were analyzed by transwell assays. (C) Cell proliferation was analyzed by EdU assay. (D) Cell apoptosis was assessed by flow cytometry. (E) HK1 and LDHA protein expression were detected by Western blotting. (F–H) Glucose consumption, lactate production, and ATP levels were analyzed by commercial kits. ∗∗ P < 0.01 and ∗∗∗ P < 0.001.

Journal: Regenerative Therapy

Article Title: WTAP stabilizes MMP12 expression to promote the malignant phenotypes of esophageal cancer cells

doi: 10.1016/j.reth.2026.101101

Figure Lengend Snippet: MMP12 knockdown inhibited the migration, invasion, proliferation, and glucose metabolism and induced cell apoptosis. KYSE150 cells were transfected with si-MMP12 or si-NC. (A and B) Cell migration and invasion were analyzed by transwell assays. (C) Cell proliferation was analyzed by EdU assay. (D) Cell apoptosis was assessed by flow cytometry. (E) HK1 and LDHA protein expression were detected by Western blotting. (F–H) Glucose consumption, lactate production, and ATP levels were analyzed by commercial kits. ∗∗ P < 0.01 and ∗∗∗ P < 0.001.

Article Snippet: Apoptosis was evaluated using a Double Staining Apoptosis Kit (Vazyme Biotech, Nanjing, China) following the protocol for Annexin V-FITC and propidium iodide dual staining.

Techniques: Knockdown, Migration, Transfection, EdU Assay, Flow Cytometry, Expressing, Western Blot

WTAP knockdown inhibited the migration, invasion, proliferation, and glucose metabolism and induced cell apoptosis by regulating MMP12 expression. KYSE150 cells were transfected with si-WTAP, MMP12 overexpression plasmid, or the matched control (si-NC and oe-NC). (A) MMP12 protein expression was detected by Western blotting. (B and C) Cell migration and invasion were analyzed by transwell assays. (D and E) Cell proliferation was analyzed by EdU assay. (F) Cell apoptosis was assessed by flow cytometry. (G and H) HK1 and LDHA protein expression were detected by Western blotting. (I–K) Glucose consumption, lactate production, and ATP levels were analyzed by commercial kits. ns: not significant, ∗ P < 0.05, ∗∗ P < 0.01 and ∗∗∗ P < 0.001.

Journal: Regenerative Therapy

Article Title: WTAP stabilizes MMP12 expression to promote the malignant phenotypes of esophageal cancer cells

doi: 10.1016/j.reth.2026.101101

Figure Lengend Snippet: WTAP knockdown inhibited the migration, invasion, proliferation, and glucose metabolism and induced cell apoptosis by regulating MMP12 expression. KYSE150 cells were transfected with si-WTAP, MMP12 overexpression plasmid, or the matched control (si-NC and oe-NC). (A) MMP12 protein expression was detected by Western blotting. (B and C) Cell migration and invasion were analyzed by transwell assays. (D and E) Cell proliferation was analyzed by EdU assay. (F) Cell apoptosis was assessed by flow cytometry. (G and H) HK1 and LDHA protein expression were detected by Western blotting. (I–K) Glucose consumption, lactate production, and ATP levels were analyzed by commercial kits. ns: not significant, ∗ P < 0.05, ∗∗ P < 0.01 and ∗∗∗ P < 0.001.

Article Snippet: Apoptosis was evaluated using a Double Staining Apoptosis Kit (Vazyme Biotech, Nanjing, China) following the protocol for Annexin V-FITC and propidium iodide dual staining.

Techniques: Knockdown, Migration, Expressing, Transfection, Over Expression, Plasmid Preparation, Control, Western Blot, EdU Assay, Flow Cytometry

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.03.062

Figure Lengend Snippet: Roles of the CD39/CD73 axis on DUB's multidirectional protection effects in Dex-treated primary BMSCs. ( A ) ELISA for ROS clearance-related enzyme T-SOD and ROS damage biomarkers 8-OHdG, AOPP, and MDA in primary BMSCs of different groups. ( B ) Western blot and quantification for the expression of ROS clearance-related proteins in primary BMSCs of different groups. ( C ) Representative images and quantitative analysis of immunofluorescence staining for MitoSox (red) in primary BMSCs of different groups, and nuclei were stained with Hoechst (blue). ( D ) Western blot and quantification for the expression of apoptosis-related proteins in primary BMSCs of different groups. ( E ) Cellular apoptosis detection in primary BMSCs of different groups by Annexin V-FITC and PI dual-staining assessment via flow cytometry. The proportion of cells in each quadrant was indicated in the plot. ( F ) Tunel (red) staining and quantification of apoptotic cells in primary BMSCs of different groups, and nuclei were stained with DAPI (blue). ( G ) Representative images and quantitative analysis of Alizarin Red S staining for mineralization in primary BMSCs of different groups under osteogenic conditions. ( H ) Western blot and quantification for the expression of osteogenesis-related proteins in primary BMSCs of different groups. n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 50 μm (C), 25 μm (F), and 200 μm (G).

Article Snippet: The proportion of early and late apoptotic primary BMSCs under different treatment conditions was determined using an Annexin V-FITC/PI Apoptosis Detection Kit (E-CK-A211, Elabscience, Wuhan, China).

Techniques: Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Immunofluorescence, Staining, Flow Cytometry, TUNEL Assay, In Vitro

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.03.062

Figure Lengend Snippet: The effect of ADO supplements on primary BMSCs. ( A ) MTT assay for the proliferation of BMSCs treated with different doses of ADO for 2 days and 10 days under osteogenic induction conditions with or without 10 μM Dex. ( B-C ) Representative images and quantitative analysis of mineralized nodule areas by Alizarin Red S staining in primary BMSCs treated with gradient doses of ADO under osteogenic induction with or without 10 μM Dex. ( D ) Western blot and quantification for the expression of osteogenesis-related proteins in primary BMSCs of different groups. ( E ) ELISA for ROS clearance-related enzyme T-SOD and ROS damage biomarkers 8-OHdG, AOPP, and MDA in primary BMSCs of different groups. ( F ) Western blot and quantification for the expression of ROS clearance-related proteins in primary BMSCs of different groups. ( G ) Representative images and quantitative analysis of immunofluorescence staining for MitoSox (red) in primary BMSCs of different groups, and nuclei were stained with Hoechst (blue). ( H ) Western blot and quantification for the expression of apoptosis-related proteins in primary BMSCs of different groups. ( I ) Cellular apoptosis detection in primary BMSCs of different groups by Annexin V-FITC and PI dual-staining assessment via flow cytometry. The proportion of cells in each quadrant was indicated in the plot. ( J ) Tunel (red) staining and quantification of apoptotic cells in primary BMSCs of different groups, and nuclei were stained with DAPI (blue). n = 4 independent repeats by using different biological samples in each group for in vitro experiments. Data were means ± s.e.m. ∗∗ p < 0.01, ∗∗∗ p < 0.001 by one-way ANOVA. Scale bars: 200 μm (B), 50 μm (G), and 25 μm (J).

Techniques: MTT Assay, Staining, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Flow Cytometry, TUNEL Assay, In Vitro

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.03.062

Figure Lengend Snippet: Summary of the study. The schematic diagram illustrates that DUB alleviates GIOP by suppressing oxidative stress and apoptosis via the CD39/CD73/ADO axis and promotes osteogenesis via ADO/A 2b R-mediated activation of the PKA/CREB pathway. The schematic diagram was created by using BioRender.com.

Techniques: Activation Assay

Inhibition of NRF2 results in reduced proliferation and increased apoptosis in chicken PGCs. (A) Morphological observation of PGCs treated with varying concentrations of ML385. Scale bar: 50 μm. (B) Comparison of cell numbers after 3 d of culture in media containing different concentrations of ML385. Different lowercase letters indicate significant differences among groups ( p < 0.05). Based on these dose-dependent effects, the 24 μM concentration was selected for all subsequent experiments. (C and D) Analysis of cell proliferation capacity via EdU assay in ML385-PGCs and Ctrl-PGCs. Scale bar: 50 μm. (E-G) Evaluation of apoptosis levels using Annexin V and PI staining in ML385-PGCs and Ctrl-PGCs. (H and I) Detection of NRF2 protein expression in ML385-PGCs and Ctrl-PGCs by Western blotting. All data are presented as mean ± SEM from three independent biological replicates ( n = 3 per group). Statistical significance is indicated by * ( p < 0.05) and *** ( p < 0.001).

Journal: Poultry Science

Article Title: NRF2 deficiency impairs proliferation and survival of chicken primordial germ cells via oxidative stress, mitochondrial dysfunction and apoptosis

doi: 10.1016/j.psj.2026.106765

Figure Lengend Snippet: Inhibition of NRF2 results in reduced proliferation and increased apoptosis in chicken PGCs. (A) Morphological observation of PGCs treated with varying concentrations of ML385. Scale bar: 50 μm. (B) Comparison of cell numbers after 3 d of culture in media containing different concentrations of ML385. Different lowercase letters indicate significant differences among groups ( p < 0.05). Based on these dose-dependent effects, the 24 μM concentration was selected for all subsequent experiments. (C and D) Analysis of cell proliferation capacity via EdU assay in ML385-PGCs and Ctrl-PGCs. Scale bar: 50 μm. (E-G) Evaluation of apoptosis levels using Annexin V and PI staining in ML385-PGCs and Ctrl-PGCs. (H and I) Detection of NRF2 protein expression in ML385-PGCs and Ctrl-PGCs by Western blotting. All data are presented as mean ± SEM from three independent biological replicates ( n = 3 per group). Statistical significance is indicated by * ( p < 0.05) and *** ( p < 0.001).

Article Snippet: Apoptosis was assessed using the Annexin V‐FITC/PI Apoptosis Detection Kit (40302ES50, Yeasen, Shanghai, China) according to the manufacturer's instructions.

Techniques: Inhibition, Comparison, Concentration Assay, EdU Assay, Staining, Expressing, Western Blot

RNA sequencing analysis reveals aberrant expression of genes related to cell growth, cell cycle, and apoptosis induced by NRF2 inhibition. GSEA of genes related to cell growth (A), cell cycle (B), and apoptosis (C and D) in ML385-PGCs and Ctrl-PGCs. Heatmap (E) depicting the expression of apoptosis pathway genes between ML385-PGCs and Ctrl-PGCs. Comparative analysis (F) of normalized FPKM values of apoptosis pathway genes between ML385-PGCs and Ctrl-PGCs. Statistical significance is indicated by * ( p < 0.05).

Journal: Poultry Science

Article Title: NRF2 deficiency impairs proliferation and survival of chicken primordial germ cells via oxidative stress, mitochondrial dysfunction and apoptosis

doi: 10.1016/j.psj.2026.106765

Figure Lengend Snippet: RNA sequencing analysis reveals aberrant expression of genes related to cell growth, cell cycle, and apoptosis induced by NRF2 inhibition. GSEA of genes related to cell growth (A), cell cycle (B), and apoptosis (C and D) in ML385-PGCs and Ctrl-PGCs. Heatmap (E) depicting the expression of apoptosis pathway genes between ML385-PGCs and Ctrl-PGCs. Comparative analysis (F) of normalized FPKM values of apoptosis pathway genes between ML385-PGCs and Ctrl-PGCs. Statistical significance is indicated by * ( p < 0.05).

Article Snippet: Apoptosis was assessed using the Annexin V‐FITC/PI Apoptosis Detection Kit (40302ES50, Yeasen, Shanghai, China) according to the manufacturer's instructions.

Techniques: RNA Sequencing, Expressing, Inhibition

Schematic representation illustrating the impact of NRF2 deficiency on chicken PGCs. NRF2 plays a critical role in maintaining the normal growth of PGCs during in vitro culture by activating antioxidant pathways. NRF2 deficiency impairs antioxidant defense, leading to oxidative stress, mitochondrial damage, and increased apoptosis. Additionally, mitophagy and autophagy are activated to remove damaged organelles. Furthermore, elevated ferroptosis markers, including oxidative stress‑induced lipid peroxidation and Fe²⁺ accumulation, are observed, contributing to reduced PGC viability. Δψm denotes mitochondrial membrane potential.

Journal: Poultry Science

Article Title: NRF2 deficiency impairs proliferation and survival of chicken primordial germ cells via oxidative stress, mitochondrial dysfunction and apoptosis

doi: 10.1016/j.psj.2026.106765

Figure Lengend Snippet: Schematic representation illustrating the impact of NRF2 deficiency on chicken PGCs. NRF2 plays a critical role in maintaining the normal growth of PGCs during in vitro culture by activating antioxidant pathways. NRF2 deficiency impairs antioxidant defense, leading to oxidative stress, mitochondrial damage, and increased apoptosis. Additionally, mitophagy and autophagy are activated to remove damaged organelles. Furthermore, elevated ferroptosis markers, including oxidative stress‑induced lipid peroxidation and Fe²⁺ accumulation, are observed, contributing to reduced PGC viability. Δψm denotes mitochondrial membrane potential.

Article Snippet: Apoptosis was assessed using the Annexin V‐FITC/PI Apoptosis Detection Kit (40302ES50, Yeasen, Shanghai, China) according to the manufacturer's instructions.

Techniques: In Vitro, Membrane

In vitro therapeutic efficacy and synergy analysis of RPAE-QM in 4 T1 cells. (A) Cell viability of 4 T1 cells incubated with different formulations for 48 h determined by MTT assay. (B) The corresponding IC 50 values of the respective treatments. (C) Representative flow cytometry plots of Annexin V-FITC/PI staining for apoptosis analysis in 4 T1 cells. (D) Quantitative analysis of the total apoptotic rate. (E) Dose-response curves of free Que., free DM1, and their combination used for quantitative synergy determination. (F) The Combination Index (CI) plot as a function of Fraction affected (Fa) generated using the Chou-Talalay method; the reference line at CI = 1 indicates an additive effect, while CI < 1 indicates synergism. Data are presented as mean ± SD (n = 3). * P < 0.05, ** P < 0.01, *** P < 0.001 and **** P < 0.0001.

Journal: International Journal of Pharmaceutics: X

Article Title: A pH-responsive dual-drug nanoplatform for stromal remodeling and enhanced chemotherapy via MMP3/TGF- β inhibition

doi: 10.1016/j.ijpx.2026.100489

Figure Lengend Snippet: In vitro therapeutic efficacy and synergy analysis of RPAE-QM in 4 T1 cells. (A) Cell viability of 4 T1 cells incubated with different formulations for 48 h determined by MTT assay. (B) The corresponding IC 50 values of the respective treatments. (C) Representative flow cytometry plots of Annexin V-FITC/PI staining for apoptosis analysis in 4 T1 cells. (D) Quantitative analysis of the total apoptotic rate. (E) Dose-response curves of free Que., free DM1, and their combination used for quantitative synergy determination. (F) The Combination Index (CI) plot as a function of Fraction affected (Fa) generated using the Chou-Talalay method; the reference line at CI = 1 indicates an additive effect, while CI < 1 indicates synergism. Data are presented as mean ± SD (n = 3). * P < 0.05, ** P < 0.01, *** P < 0.001 and **** P < 0.0001.

Article Snippet: After 24 h, the cells were harvested and stained with Annexin V-FITC/PI Cell Apoptosis Detection Kit (Beyotime, China) for flow cytometer analysis.

Techniques: In Vitro, Drug discovery, Incubation, MTT Assay, Flow Cytometry, Staining, Generated

GO-EDM-DTX-Vad combined with NIR induces TNBC cell death, apoptosis and immunogenic cell death. (A, B) Calcein-AM/PI live/dead staining of 4T1 (A) and MDA-MB-231 (B) cells (live, green; dead, red; scale bar, 200 μm). (C, D) Annexin V/PI apoptosis plots for 4T1 (C) and MDA-MB-231 (D) cells. (E, F) Quantification of viable and early/late apoptotic 4T1 cells. (H, I) Quantification of viable and early/late apoptotic MDA-MB-231 cells. (G, J) Dose–response viability curves after 48 h treatment with free DTX or GO-EDM-DTX-Vad in 4T1 (G) and MDA-MB-231 (J). (K, L) Immunofluorescence of CRT exposure and HMGB1 release after 24 h treatment in 4T1 (K) and MDA-MB-231 (L) cells (nuclei, blue; CRT/HMGB1, green; scale bar, 100 μm). (M) Schematic of the ICD-to-DC maturation assay. (N–P) Frequencies of CD40 + , CD80 + and CD86 + DCs after co-culture. Data are mean ± SD (n = 3). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001; ns, not significant.

Journal: Materials Today Bio

Article Title: Mannosylated graphene oxide nanotherapeutics co-delivering docetaxel and a STING agonist reprogram myeloid cells and potentiate antitumor immunity

doi: 10.1016/j.mtbio.2026.103086

Figure Lengend Snippet: GO-EDM-DTX-Vad combined with NIR induces TNBC cell death, apoptosis and immunogenic cell death. (A, B) Calcein-AM/PI live/dead staining of 4T1 (A) and MDA-MB-231 (B) cells (live, green; dead, red; scale bar, 200 μm). (C, D) Annexin V/PI apoptosis plots for 4T1 (C) and MDA-MB-231 (D) cells. (E, F) Quantification of viable and early/late apoptotic 4T1 cells. (H, I) Quantification of viable and early/late apoptotic MDA-MB-231 cells. (G, J) Dose–response viability curves after 48 h treatment with free DTX or GO-EDM-DTX-Vad in 4T1 (G) and MDA-MB-231 (J). (K, L) Immunofluorescence of CRT exposure and HMGB1 release after 24 h treatment in 4T1 (K) and MDA-MB-231 (L) cells (nuclei, blue; CRT/HMGB1, green; scale bar, 100 μm). (M) Schematic of the ICD-to-DC maturation assay. (N–P) Frequencies of CD40 + , CD80 + and CD86 + DCs after co-culture. Data are mean ± SD (n = 3). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001; ns, not significant.

Article Snippet: Annexin V-FITC/PI apoptosis detection kits were purchased from Elabscience Biotechnology Co., Ltd. (Wuhan, China).

Techniques: Staining, Immunofluorescence, Co-Culture Assay

Agrimol B induces mitochondrial damage in PDAC cells. (A) Results of label-free quantitative proteomics after Agrimol B treatment for 24 h. (B) Western blot analysis of HADHA, TIM23, and SOD2 in PANC-1 and AsPC-1 cells. (C) Flow cytometric analysis of Fluo-4 AM accumulation in cells treated with or without 45 μmol/l Agrimol B. (D) Representative images of Fluo-4 AM accumulation in PANC-1 and AsPC-1 cells treated with or without 45 μmol/l Agrimol B for 24 h. Scale bars, 10 μm. (E) Flow cytometric analysis of mitochondrial ROS accumulation in cells treated with or without 45 μmol/l Agrimol B. (F) Representative images of mitochondrial morphology stained with Annexin V-FITC and MitoTracker Red CMXRos in PANC-1 and AsPC-1 cells treated with or without 45 μmol/l Agrimol B for 24 h. Scale bars, 10 μm. (G) Quantitative RT-PCR analysis of mtDNA copies. (H) ATP levels in PANC-1 and AsPC-1 cells treated with or without 45 μmol/l Agrimol B for 24 h. (I) Mitochondrial morphology was observed via transmission electron microscopy after treatment with or without Agrimol B for 24 h. Scale bars, 500 nm.

Journal: Precision Clinical Medicine

Article Title: Agrimol B inhibits pancreatic ductal adenocarcinoma by induction of lethal mitophagy through decreasing mitochondrial transcription termination factor 3

doi: 10.1093/pcmedi/pbag009

Figure Lengend Snippet: Agrimol B induces mitochondrial damage in PDAC cells. (A) Results of label-free quantitative proteomics after Agrimol B treatment for 24 h. (B) Western blot analysis of HADHA, TIM23, and SOD2 in PANC-1 and AsPC-1 cells. (C) Flow cytometric analysis of Fluo-4 AM accumulation in cells treated with or without 45 μmol/l Agrimol B. (D) Representative images of Fluo-4 AM accumulation in PANC-1 and AsPC-1 cells treated with or without 45 μmol/l Agrimol B for 24 h. Scale bars, 10 μm. (E) Flow cytometric analysis of mitochondrial ROS accumulation in cells treated with or without 45 μmol/l Agrimol B. (F) Representative images of mitochondrial morphology stained with Annexin V-FITC and MitoTracker Red CMXRos in PANC-1 and AsPC-1 cells treated with or without 45 μmol/l Agrimol B for 24 h. Scale bars, 10 μm. (G) Quantitative RT-PCR analysis of mtDNA copies. (H) ATP levels in PANC-1 and AsPC-1 cells treated with or without 45 μmol/l Agrimol B for 24 h. (I) Mitochondrial morphology was observed via transmission electron microscopy after treatment with or without Agrimol B for 24 h. Scale bars, 500 nm.

Article Snippet: The apoptotic ratio was determined via an Annexin V-FITC/PI Apoptosis Detection Kit (4A BIOTECH) according to the manufacturer’s protocol.

Techniques: Quantitative Proteomics, Western Blot, Staining, Quantitative RT-PCR, Transmission Assay, Electron Microscopy

Exosomes derived from low-passage DPCs regulated HFSC proliferation. (A) Indirect immunofluorescence showing ALPL and PCNA expression in low-passage (P1) and high-passage (P8) DPCs (scale bar = 50 μm). (B) RT-qPCR analysis of HF development-related gene expression in P1 and P8 DPCs (unpaired two-tailed t -test, n = 3). (C) TEM images of exosomes from P1 DPCs (DPC-Exos P1) and P8 DPCs (DPC-Exos P8). (D) NTA measurement of particle size of DPC-Exos P1 and DPC-Exos P8. (E) Western blot detection of exosome-specific proteins in DPC-Exos P1 and DPC-Exos P8. (F) CCK-8 assay evaluating HFSC proliferation after treatment with DPC-Exos from P1 and P8 (one-way ANOVA, n = 5). (G) Flow cytometry analysis of HFSC apoptosis after treatment with DPC-Exos from P1 and P8 (one-way ANOVA, n = 3). ∗ P < 0.05, ∗∗ P < 0.01.

Journal: Non-coding RNA Research

Article Title: Exosomal miRNA-218–5p derived from low-passage dermal papilla cells modulates hair follicle growth and development

doi: 10.1016/j.ncrna.2026.01.004

Figure Lengend Snippet: Exosomes derived from low-passage DPCs regulated HFSC proliferation. (A) Indirect immunofluorescence showing ALPL and PCNA expression in low-passage (P1) and high-passage (P8) DPCs (scale bar = 50 μm). (B) RT-qPCR analysis of HF development-related gene expression in P1 and P8 DPCs (unpaired two-tailed t -test, n = 3). (C) TEM images of exosomes from P1 DPCs (DPC-Exos P1) and P8 DPCs (DPC-Exos P8). (D) NTA measurement of particle size of DPC-Exos P1 and DPC-Exos P8. (E) Western blot detection of exosome-specific proteins in DPC-Exos P1 and DPC-Exos P8. (F) CCK-8 assay evaluating HFSC proliferation after treatment with DPC-Exos from P1 and P8 (one-way ANOVA, n = 5). (G) Flow cytometry analysis of HFSC apoptosis after treatment with DPC-Exos from P1 and P8 (one-way ANOVA, n = 3). ∗ P < 0.05, ∗∗ P < 0.01.

Article Snippet: The Annexin V-FITC Apoptosis Detection Kit (Vazyme, China, Cat No. A214) was employed, and apoptosis rates were analyzed via flow cytometry using a FACSAria SORP instrument (Becton Dickinson, USA).

Techniques: Derivative Assay, Immunofluorescence, Expressing, Quantitative RT-PCR, Gene Expression, Two Tailed Test, Western Blot, CCK-8 Assay, Flow Cytometry

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