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cfda se  (MedChemExpress)


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    Structured Review

    MedChemExpress cfda se
    In vitro therapeutic effect of aCD47-CATE. (A) The cell viability of Hepa1-6 cells after different treatments (100 μg/mL), as determined by CCK-8 assay (n = 5). (B) Confocal laser scanning microscopy (CLSM) images of TUNEL staining (red) in Hepa1-6 cells. Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. (C) Quantitative analysis of the TUNEL-positive cells from (B). Data are presented as mean ± SD (n = 3). (D) Flow cytometry analysis of apoptosis in Hepa1-6 cells after different treatments (n = 3). (E) Flow cytometric analysis of the M1 macrophage marker CD80 in RAW264.7 cells after co-culture with conditioned media from the treated Hepa1-6 cells. (F) CLSM images showing the infiltration of <t>CFDA-SE-labeled</t> M1 macrophages (green) into Hepa1-6 tumor spheroids. Scale bar = 200 μm. (G) Quantitative analysis of the fluorescence intensity of infiltrated macrophages in (F). Data are presented as mean ± SD (n = 3). ns P > 0.05; ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001,∗∗∗∗p < 0.0001.
    Cfda Se, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 162 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    cfda se - by Bioz Stars, 2026-08
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    Images

    1) Product Images from "Macrophage exosome-engineered nanoplatform with pH-responsive ratiometric photoacoustic and NIR-II fluorescence imaging for guided photothermal immunotherapy of hepatocellular carcinoma"

    Article Title: Macrophage exosome-engineered nanoplatform with pH-responsive ratiometric photoacoustic and NIR-II fluorescence imaging for guided photothermal immunotherapy of hepatocellular carcinoma

    Journal: Materials Today Bio

    doi: 10.1016/j.mtbio.2026.103058

    In vitro therapeutic effect of aCD47-CATE. (A) The cell viability of Hepa1-6 cells after different treatments (100 μg/mL), as determined by CCK-8 assay (n = 5). (B) Confocal laser scanning microscopy (CLSM) images of TUNEL staining (red) in Hepa1-6 cells. Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. (C) Quantitative analysis of the TUNEL-positive cells from (B). Data are presented as mean ± SD (n = 3). (D) Flow cytometry analysis of apoptosis in Hepa1-6 cells after different treatments (n = 3). (E) Flow cytometric analysis of the M1 macrophage marker CD80 in RAW264.7 cells after co-culture with conditioned media from the treated Hepa1-6 cells. (F) CLSM images showing the infiltration of CFDA-SE-labeled M1 macrophages (green) into Hepa1-6 tumor spheroids. Scale bar = 200 μm. (G) Quantitative analysis of the fluorescence intensity of infiltrated macrophages in (F). Data are presented as mean ± SD (n = 3). ns P > 0.05; ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001,∗∗∗∗p < 0.0001.
    Figure Legend Snippet: In vitro therapeutic effect of aCD47-CATE. (A) The cell viability of Hepa1-6 cells after different treatments (100 μg/mL), as determined by CCK-8 assay (n = 5). (B) Confocal laser scanning microscopy (CLSM) images of TUNEL staining (red) in Hepa1-6 cells. Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. (C) Quantitative analysis of the TUNEL-positive cells from (B). Data are presented as mean ± SD (n = 3). (D) Flow cytometry analysis of apoptosis in Hepa1-6 cells after different treatments (n = 3). (E) Flow cytometric analysis of the M1 macrophage marker CD80 in RAW264.7 cells after co-culture with conditioned media from the treated Hepa1-6 cells. (F) CLSM images showing the infiltration of CFDA-SE-labeled M1 macrophages (green) into Hepa1-6 tumor spheroids. Scale bar = 200 μm. (G) Quantitative analysis of the fluorescence intensity of infiltrated macrophages in (F). Data are presented as mean ± SD (n = 3). ns P > 0.05; ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001,∗∗∗∗p < 0.0001.

    Techniques Used: In Vitro, CCK-8 Assay, Confocal Laser Scanning Microscopy, TUNEL Assay, Staining, Flow Cytometry, Marker, Co-Culture Assay, Labeling, Fluorescence



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    Neutralization of merozoites. A Purification of infected erythrocytes using the Percoll separation solution, displaying infected (black arrow) and normal (red arrow) erythrocytes. B Confocal fluorescent images of merozoites (blue), PECm-Allicin@LM (red), and their colocalization (purple). Scale bar = 50 μm. C Representative scatter plots of Hoechst <t>33342/CFDA-SE</t> for the invasion test of merozoites and normal erythrocytes after drug treatment. D Intrusion rate (the percentage of cells in the Q2 area in each group relative to that in the Q2 area in the Model group). Data are presented as mean ± SEM ( n = 3), * P < 0.05. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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    In vitro therapeutic effect of aCD47-CATE. (A) The cell viability of Hepa1-6 cells after different treatments (100 μg/mL), as determined by CCK-8 assay (n = 5). (B) Confocal laser scanning microscopy (CLSM) images of TUNEL staining (red) in Hepa1-6 cells. Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. (C) Quantitative analysis of the TUNEL-positive cells from (B). Data are presented as mean ± SD (n = 3). (D) Flow cytometry analysis of apoptosis in Hepa1-6 cells after different treatments (n = 3). (E) Flow cytometric analysis of the M1 macrophage marker CD80 in RAW264.7 cells after co-culture with conditioned media from the treated Hepa1-6 cells. (F) CLSM images showing the infiltration of <t>CFDA-SE-labeled</t> M1 macrophages (green) into Hepa1-6 tumor spheroids. Scale bar = 200 μm. (G) Quantitative analysis of the fluorescence intensity of infiltrated macrophages in (F). Data are presented as mean ± SD (n = 3). ns P > 0.05; ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001,∗∗∗∗p < 0.0001.
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    ( A to H ) Single cells were isolated from fresh cancer or adjacent normal tissues. Cells were labeled with anti-CD4 and anti-TCR antibodies, followed by intracellular anti-FOXP3 and anti-SRSF3 labeling. [(A) and (E)] Gating strategy to identify TCR + CD4 + FOXP3 + T reg cells and representative fluorescence-activated cell sorting (FACS) plots showing the expression levels of FOXP3 and SRSF3 in T reg cells isolated from oral squamous cell carcinoma (A) and breast cancer (E) or their adjacent normal tissues, respectively. [(B) and (F)] Summary of SRSF3-positive population percentage of T reg cells in oral squamous cell carcinoma (A) or breast cancer (E) tissues. [(C), (D), (G), and (H)] Summary of FOXP3 and SRSF3 MFI of T reg cells in oral squamous cell carcinoma [(C) and (D)] ( n = 5) or breast cancer [(G) and (H)] ( n = 8) tissues. Data are mean ± SEM. ( I ) Human T reg cells were purified from PBMCs and then transfected with siRNA [anti-SRSF3 or nonspecific (NS)]. PBMCs from the same donor were labeled by <t>CFSE</t> and mixed with T reg cells as the indicated ratio. Cells were cultured for 4 days in the presence of anti-human CD3 antibody (0.5 μg/ml). Then, cells were stained with an anti-CD8 antibody. The proliferation of CD8 + cells was measured by FACS. Data are mean ± SEM, n = 3. ( J ) Down-regulation of SRSF3 released the inhibition of T reg cell on the expression of TNF-α, IFN-γ, and IL-2 by CD8 + T cells. The expression levels of TNF-α, IFN-γ, and IL-2 in CD8 + T cells after in vitro suppression assay were analyzed by intracellular cytokine staining and FACS. Data are mean ± SEM, n = 5. P values are from a two-sided unpaired t test [(I) and (J)] or a paired t test [(B), (C), (D), (F), (G), and (H)].
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    Combined treatment with LAG3pep-2 and anti-programmed death-ligand 1 (anti-PD-L1) antibody restores T cell activity against tumor cells. (A) Experimental schemes. CD8+ T cells were isolated from the spleen of MC38 tumor-bearing mice and incubated for 48 h with anti-CD3/CD28 beads (activation) and interleukin-2 (IL-2)/interleukin-15 (IL-15) (proliferation). The activated T cells were co-cultured with MC38 cells in the absence or presence of LAG3pep-2 and anti-mouse PD-L1 antibody alone or in combination. Created with BioRender.com . (B) Activated CD8+ T cells were stained with <t>carboxyfluorescein</t> <t>succinimidyl</t> ester <t>(CFSE)</t> dye and co-cultured with tumor cells for 24 h. The population of CD3+/CFSE− cells was measured. (C to E) After co-culturing for 24 h, the culture medium was collected, and the percentage of cell death (lactate dehydrogenase [LDH] release) (C) and the concentrations of interferon-γ (IFN-γ) (D) and granzyme B (E) were measured. Data are presented as the mean ± SD of 3 independent experiments. * P < 0.05; ** P < 0.01; *** P < 0.001; ns, not significant by one-way analysis of variance (ANOVA).
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    Image Search Results


    Neutralization of merozoites. A Purification of infected erythrocytes using the Percoll separation solution, displaying infected (black arrow) and normal (red arrow) erythrocytes. B Confocal fluorescent images of merozoites (blue), PECm-Allicin@LM (red), and their colocalization (purple). Scale bar = 50 μm. C Representative scatter plots of Hoechst 33342/CFDA-SE for the invasion test of merozoites and normal erythrocytes after drug treatment. D Intrusion rate (the percentage of cells in the Q2 area in each group relative to that in the Q2 area in the Model group). Data are presented as mean ± SEM ( n = 3), * P < 0.05. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Journal: International Journal of Pharmaceutics: X

    Article Title: Allicin-based biomimetic nanoparticles of the erythrocyte membrane for the delivery of lumefantrine to enhance its antimalarial effect

    doi: 10.1016/j.ijpx.2026.100487

    Figure Lengend Snippet: Neutralization of merozoites. A Purification of infected erythrocytes using the Percoll separation solution, displaying infected (black arrow) and normal (red arrow) erythrocytes. B Confocal fluorescent images of merozoites (blue), PECm-Allicin@LM (red), and their colocalization (purple). Scale bar = 50 μm. C Representative scatter plots of Hoechst 33342/CFDA-SE for the invasion test of merozoites and normal erythrocytes after drug treatment. D Intrusion rate (the percentage of cells in the Q2 area in each group relative to that in the Q2 area in the Model group). Data are presented as mean ± SEM ( n = 3), * P < 0.05. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Article Snippet: 5–6(and 6)-carboxyfuorescein diacetate, succinimidyl ester (CFDA-SE) was purchased from Yeasen Biotechnology (Shanghai) Co., Ltd. (China).

    Techniques: Neutralization, Purification, Infection

    In vitro therapeutic effect of aCD47-CATE. (A) The cell viability of Hepa1-6 cells after different treatments (100 μg/mL), as determined by CCK-8 assay (n = 5). (B) Confocal laser scanning microscopy (CLSM) images of TUNEL staining (red) in Hepa1-6 cells. Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. (C) Quantitative analysis of the TUNEL-positive cells from (B). Data are presented as mean ± SD (n = 3). (D) Flow cytometry analysis of apoptosis in Hepa1-6 cells after different treatments (n = 3). (E) Flow cytometric analysis of the M1 macrophage marker CD80 in RAW264.7 cells after co-culture with conditioned media from the treated Hepa1-6 cells. (F) CLSM images showing the infiltration of CFDA-SE-labeled M1 macrophages (green) into Hepa1-6 tumor spheroids. Scale bar = 200 μm. (G) Quantitative analysis of the fluorescence intensity of infiltrated macrophages in (F). Data are presented as mean ± SD (n = 3). ns P > 0.05; ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001,∗∗∗∗p < 0.0001.

    Journal: Materials Today Bio

    Article Title: Macrophage exosome-engineered nanoplatform with pH-responsive ratiometric photoacoustic and NIR-II fluorescence imaging for guided photothermal immunotherapy of hepatocellular carcinoma

    doi: 10.1016/j.mtbio.2026.103058

    Figure Lengend Snippet: In vitro therapeutic effect of aCD47-CATE. (A) The cell viability of Hepa1-6 cells after different treatments (100 μg/mL), as determined by CCK-8 assay (n = 5). (B) Confocal laser scanning microscopy (CLSM) images of TUNEL staining (red) in Hepa1-6 cells. Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. (C) Quantitative analysis of the TUNEL-positive cells from (B). Data are presented as mean ± SD (n = 3). (D) Flow cytometry analysis of apoptosis in Hepa1-6 cells after different treatments (n = 3). (E) Flow cytometric analysis of the M1 macrophage marker CD80 in RAW264.7 cells after co-culture with conditioned media from the treated Hepa1-6 cells. (F) CLSM images showing the infiltration of CFDA-SE-labeled M1 macrophages (green) into Hepa1-6 tumor spheroids. Scale bar = 200 μm. (G) Quantitative analysis of the fluorescence intensity of infiltrated macrophages in (F). Data are presented as mean ± SD (n = 3). ns P > 0.05; ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001,∗∗∗∗p < 0.0001.

    Article Snippet: RAW264.7 cells were labeled with 1 μM CFDA-SE (Medchemexpress), added to the 96-well plate, and co-cultured with the spheroids for 6 h. The cell pellet was aspirated, fixed with 4% paraformaldehyde, stained with DAPI for 5 min, and observed under a fluorescence microscope (Leica, 3D thunder).

    Techniques: In Vitro, CCK-8 Assay, Confocal Laser Scanning Microscopy, TUNEL Assay, Staining, Flow Cytometry, Marker, Co-Culture Assay, Labeling, Fluorescence

    ( A to H ) Single cells were isolated from fresh cancer or adjacent normal tissues. Cells were labeled with anti-CD4 and anti-TCR antibodies, followed by intracellular anti-FOXP3 and anti-SRSF3 labeling. [(A) and (E)] Gating strategy to identify TCR + CD4 + FOXP3 + T reg cells and representative fluorescence-activated cell sorting (FACS) plots showing the expression levels of FOXP3 and SRSF3 in T reg cells isolated from oral squamous cell carcinoma (A) and breast cancer (E) or their adjacent normal tissues, respectively. [(B) and (F)] Summary of SRSF3-positive population percentage of T reg cells in oral squamous cell carcinoma (A) or breast cancer (E) tissues. [(C), (D), (G), and (H)] Summary of FOXP3 and SRSF3 MFI of T reg cells in oral squamous cell carcinoma [(C) and (D)] ( n = 5) or breast cancer [(G) and (H)] ( n = 8) tissues. Data are mean ± SEM. ( I ) Human T reg cells were purified from PBMCs and then transfected with siRNA [anti-SRSF3 or nonspecific (NS)]. PBMCs from the same donor were labeled by CFSE and mixed with T reg cells as the indicated ratio. Cells were cultured for 4 days in the presence of anti-human CD3 antibody (0.5 μg/ml). Then, cells were stained with an anti-CD8 antibody. The proliferation of CD8 + cells was measured by FACS. Data are mean ± SEM, n = 3. ( J ) Down-regulation of SRSF3 released the inhibition of T reg cell on the expression of TNF-α, IFN-γ, and IL-2 by CD8 + T cells. The expression levels of TNF-α, IFN-γ, and IL-2 in CD8 + T cells after in vitro suppression assay were analyzed by intracellular cytokine staining and FACS. Data are mean ± SEM, n = 5. P values are from a two-sided unpaired t test [(I) and (J)] or a paired t test [(B), (C), (D), (F), (G), and (H)].

    Journal: Science Advances

    Article Title: SRSF3 determines T reg cell fate in antitumor immunity and autoimmunity

    doi: 10.1126/sciadv.aeh1671

    Figure Lengend Snippet: ( A to H ) Single cells were isolated from fresh cancer or adjacent normal tissues. Cells were labeled with anti-CD4 and anti-TCR antibodies, followed by intracellular anti-FOXP3 and anti-SRSF3 labeling. [(A) and (E)] Gating strategy to identify TCR + CD4 + FOXP3 + T reg cells and representative fluorescence-activated cell sorting (FACS) plots showing the expression levels of FOXP3 and SRSF3 in T reg cells isolated from oral squamous cell carcinoma (A) and breast cancer (E) or their adjacent normal tissues, respectively. [(B) and (F)] Summary of SRSF3-positive population percentage of T reg cells in oral squamous cell carcinoma (A) or breast cancer (E) tissues. [(C), (D), (G), and (H)] Summary of FOXP3 and SRSF3 MFI of T reg cells in oral squamous cell carcinoma [(C) and (D)] ( n = 5) or breast cancer [(G) and (H)] ( n = 8) tissues. Data are mean ± SEM. ( I ) Human T reg cells were purified from PBMCs and then transfected with siRNA [anti-SRSF3 or nonspecific (NS)]. PBMCs from the same donor were labeled by CFSE and mixed with T reg cells as the indicated ratio. Cells were cultured for 4 days in the presence of anti-human CD3 antibody (0.5 μg/ml). Then, cells were stained with an anti-CD8 antibody. The proliferation of CD8 + cells was measured by FACS. Data are mean ± SEM, n = 3. ( J ) Down-regulation of SRSF3 released the inhibition of T reg cell on the expression of TNF-α, IFN-γ, and IL-2 by CD8 + T cells. The expression levels of TNF-α, IFN-γ, and IL-2 in CD8 + T cells after in vitro suppression assay were analyzed by intracellular cytokine staining and FACS. Data are mean ± SEM, n = 5. P values are from a two-sided unpaired t test [(I) and (J)] or a paired t test [(B), (C), (D), (F), (G), and (H)].

    Article Snippet: PBMCs from the same donor were labeled by carboxyfluorescein diacetate succinimidyl ester (CFSE; 1 μg/ml; Invitrogen) and mixed with T reg cells at various ratios in round-bottomed 96-well plates.

    Techniques: Isolation, Labeling, Fluorescence, FACS, Expressing, Purification, Transfection, Cell Culture, Staining, Inhibition, In Vitro, Suppression Assay

    Combined treatment with LAG3pep-2 and anti-programmed death-ligand 1 (anti-PD-L1) antibody restores T cell activity against tumor cells. (A) Experimental schemes. CD8+ T cells were isolated from the spleen of MC38 tumor-bearing mice and incubated for 48 h with anti-CD3/CD28 beads (activation) and interleukin-2 (IL-2)/interleukin-15 (IL-15) (proliferation). The activated T cells were co-cultured with MC38 cells in the absence or presence of LAG3pep-2 and anti-mouse PD-L1 antibody alone or in combination. Created with BioRender.com . (B) Activated CD8+ T cells were stained with carboxyfluorescein succinimidyl ester (CFSE) dye and co-cultured with tumor cells for 24 h. The population of CD3+/CFSE− cells was measured. (C to E) After co-culturing for 24 h, the culture medium was collected, and the percentage of cell death (lactate dehydrogenase [LDH] release) (C) and the concentrations of interferon-γ (IFN-γ) (D) and granzyme B (E) were measured. Data are presented as the mean ± SD of 3 independent experiments. * P < 0.05; ** P < 0.01; *** P < 0.001; ns, not significant by one-way analysis of variance (ANOVA).

    Journal: Biomaterials Research

    Article Title: A Peptide Inhibitor of Lymphocyte Activation Gene-3 Interaction with Fibrinogen-like Protein 1 Synergizes with Programmed Death-Ligand 1 Blockade to Restore T Cell Activity and Inhibit Tumor Growth

    doi: 10.34133/bmr.0364

    Figure Lengend Snippet: Combined treatment with LAG3pep-2 and anti-programmed death-ligand 1 (anti-PD-L1) antibody restores T cell activity against tumor cells. (A) Experimental schemes. CD8+ T cells were isolated from the spleen of MC38 tumor-bearing mice and incubated for 48 h with anti-CD3/CD28 beads (activation) and interleukin-2 (IL-2)/interleukin-15 (IL-15) (proliferation). The activated T cells were co-cultured with MC38 cells in the absence or presence of LAG3pep-2 and anti-mouse PD-L1 antibody alone or in combination. Created with BioRender.com . (B) Activated CD8+ T cells were stained with carboxyfluorescein succinimidyl ester (CFSE) dye and co-cultured with tumor cells for 24 h. The population of CD3+/CFSE− cells was measured. (C to E) After co-culturing for 24 h, the culture medium was collected, and the percentage of cell death (lactate dehydrogenase [LDH] release) (C) and the concentrations of interferon-γ (IFN-γ) (D) and granzyme B (E) were measured. Data are presented as the mean ± SD of 3 independent experiments. * P < 0.05; ** P < 0.01; *** P < 0.001; ns, not significant by one-way analysis of variance (ANOVA).

    Article Snippet: The CD8+ T cells were stained with 5 μM of carboxyfluorescein succinimidyl ester (CFSE) dye (Thermo Fisher Scientific) in an incubator at 37 °C for 20 min and then co-cultured with tumor cells for 24 h. Next, cell proliferation was examined by counting the CD3+ T cells using a flow cytometer.

    Techniques: Activity Assay, Isolation, Incubation, Activation Assay, Cell Culture, Staining