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Servicebio Inc ki67 immunohistochemistry
GZMA-F2R interaction mediates STNvac efficacy through T cell activation (A) Bubble plot showing ligand-receptor pairs between ISG15 + CD8 + T cells and APCs (B cells, CD4 + T cells, and DCs). (B) Violin plots showing F2R expression across T cell subsets and GZMA expression in APCs. (C and D) Therapeutic evaluation of STNvac co-administration with F2R antagonist (F2RA, SCH79797 ) ( n = 7 mice per group). (C) Bioluminescence images showing tumor burden in orthotopic HCC-bearing mice under the indicated treatments. (D) Survival curves of mice in different groups. (E and F) Multicolor immunofluorescence staining of intratumoral <t>Ki67</t> + CD69 + ISG15 + CD8 + T cells. (E) Representative images. Scale bars, 20 μm. (F) Quantitative analysis of positive cell density in five randomly selected areas per tumor section. (G and H) Activation of human HCC TILs through the GZMA-F2R interaction. (G) Schematic illustration of the treatment schedule. (H) Quantitative analysis of 41BB + CD3 + CD8 + T cells after 24 h of GZMA stimulation ( n = 2 biological replicates, each analyzed in triplicate). Statistics: one-way ANOVA for (F) and (H); log rank (Mantel-Cox) test for (D). Mean ± SD. Significance levels: ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001. See also and .
Ki67 Immunohistochemistry, supplied by Servicebio Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 86 stars, based on 1 article reviews
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1) Product Images from "Spleen-targeted neoantigen mRNA vaccine induces ISG15 + CD8 + T cell-mediated tertiary lymphoid structure formation in hepatocellular carcinoma"

Article Title: Spleen-targeted neoantigen mRNA vaccine induces ISG15 + CD8 + T cell-mediated tertiary lymphoid structure formation in hepatocellular carcinoma

Journal: Cell Reports Medicine

doi: 10.1016/j.xcrm.2026.102754

GZMA-F2R interaction mediates STNvac efficacy through T cell activation (A) Bubble plot showing ligand-receptor pairs between ISG15 + CD8 + T cells and APCs (B cells, CD4 + T cells, and DCs). (B) Violin plots showing F2R expression across T cell subsets and GZMA expression in APCs. (C and D) Therapeutic evaluation of STNvac co-administration with F2R antagonist (F2RA, SCH79797 ) ( n = 7 mice per group). (C) Bioluminescence images showing tumor burden in orthotopic HCC-bearing mice under the indicated treatments. (D) Survival curves of mice in different groups. (E and F) Multicolor immunofluorescence staining of intratumoral Ki67 + CD69 + ISG15 + CD8 + T cells. (E) Representative images. Scale bars, 20 μm. (F) Quantitative analysis of positive cell density in five randomly selected areas per tumor section. (G and H) Activation of human HCC TILs through the GZMA-F2R interaction. (G) Schematic illustration of the treatment schedule. (H) Quantitative analysis of 41BB + CD3 + CD8 + T cells after 24 h of GZMA stimulation ( n = 2 biological replicates, each analyzed in triplicate). Statistics: one-way ANOVA for (F) and (H); log rank (Mantel-Cox) test for (D). Mean ± SD. Significance levels: ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001. See also and .
Figure Legend Snippet: GZMA-F2R interaction mediates STNvac efficacy through T cell activation (A) Bubble plot showing ligand-receptor pairs between ISG15 + CD8 + T cells and APCs (B cells, CD4 + T cells, and DCs). (B) Violin plots showing F2R expression across T cell subsets and GZMA expression in APCs. (C and D) Therapeutic evaluation of STNvac co-administration with F2R antagonist (F2RA, SCH79797 ) ( n = 7 mice per group). (C) Bioluminescence images showing tumor burden in orthotopic HCC-bearing mice under the indicated treatments. (D) Survival curves of mice in different groups. (E and F) Multicolor immunofluorescence staining of intratumoral Ki67 + CD69 + ISG15 + CD8 + T cells. (E) Representative images. Scale bars, 20 μm. (F) Quantitative analysis of positive cell density in five randomly selected areas per tumor section. (G and H) Activation of human HCC TILs through the GZMA-F2R interaction. (G) Schematic illustration of the treatment schedule. (H) Quantitative analysis of 41BB + CD3 + CD8 + T cells after 24 h of GZMA stimulation ( n = 2 biological replicates, each analyzed in triplicate). Statistics: one-way ANOVA for (F) and (H); log rank (Mantel-Cox) test for (D). Mean ± SD. Significance levels: ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001. See also and .

Techniques Used: Activation Assay, Expressing, Multicolor Immunofluorescence Staining

Related Articles

Immunohistochemistry:

Article Title: Spleen-targeted neoantigen mRNA vaccine induces ISG15 + CD8 + T cell-mediated tertiary lymphoid structure formation in hepatocellular carcinoma
Article Snippet: Hematoxylin and eosin (H&E) staining was performed using H&E Stain Kit (Solarbio) for histopathology analysis. .. Ki67 immunohistochemistry (Servicebio) and TUNEL assays (One Step TUNEL Apoptosis Assay Kit, Beyotime) were conducted to evaluate tumor cell proliferation and apoptosis. .. For two-color immunofluorescence, sections were stained with anti-CD4 (Servicebio) and anti-CD8 (Servicebio) antibodies to visualize intratumoral T cell infiltration.

TUNEL Assay:

Article Title: Spleen-targeted neoantigen mRNA vaccine induces ISG15 + CD8 + T cell-mediated tertiary lymphoid structure formation in hepatocellular carcinoma
Article Snippet: Hematoxylin and eosin (H&E) staining was performed using H&E Stain Kit (Solarbio) for histopathology analysis. .. Ki67 immunohistochemistry (Servicebio) and TUNEL assays (One Step TUNEL Apoptosis Assay Kit, Beyotime) were conducted to evaluate tumor cell proliferation and apoptosis. .. For two-color immunofluorescence, sections were stained with anti-CD4 (Servicebio) and anti-CD8 (Servicebio) antibodies to visualize intratumoral T cell infiltration.

Apoptosis Assay:

Article Title: Spleen-targeted neoantigen mRNA vaccine induces ISG15 + CD8 + T cell-mediated tertiary lymphoid structure formation in hepatocellular carcinoma
Article Snippet: Hematoxylin and eosin (H&E) staining was performed using H&E Stain Kit (Solarbio) for histopathology analysis. .. Ki67 immunohistochemistry (Servicebio) and TUNEL assays (One Step TUNEL Apoptosis Assay Kit, Beyotime) were conducted to evaluate tumor cell proliferation and apoptosis. .. For two-color immunofluorescence, sections were stained with anti-CD4 (Servicebio) and anti-CD8 (Servicebio) antibodies to visualize intratumoral T cell infiltration.



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Servicebio Inc ki67 immunohistochemistry
GZMA-F2R interaction mediates STNvac efficacy through T cell activation (A) Bubble plot showing ligand-receptor pairs between ISG15 + CD8 + T cells and APCs (B cells, CD4 + T cells, and DCs). (B) Violin plots showing F2R expression across T cell subsets and GZMA expression in APCs. (C and D) Therapeutic evaluation of STNvac co-administration with F2R antagonist (F2RA, SCH79797 ) ( n = 7 mice per group). (C) Bioluminescence images showing tumor burden in orthotopic HCC-bearing mice under the indicated treatments. (D) Survival curves of mice in different groups. (E and F) Multicolor immunofluorescence staining of intratumoral <t>Ki67</t> + CD69 + ISG15 + CD8 + T cells. (E) Representative images. Scale bars, 20 μm. (F) Quantitative analysis of positive cell density in five randomly selected areas per tumor section. (G and H) Activation of human HCC TILs through the GZMA-F2R interaction. (G) Schematic illustration of the treatment schedule. (H) Quantitative analysis of 41BB + CD3 + CD8 + T cells after 24 h of GZMA stimulation ( n = 2 biological replicates, each analyzed in triplicate). Statistics: one-way ANOVA for (F) and (H); log rank (Mantel-Cox) test for (D). Mean ± SD. Significance levels: ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001. See also and .
Ki67 Immunohistochemistry, supplied by Servicebio Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Servicebio Inc ki67 immunohistochemistry kit
GZMA-F2R interaction mediates STNvac efficacy through T cell activation (A) Bubble plot showing ligand-receptor pairs between ISG15 + CD8 + T cells and APCs (B cells, CD4 + T cells, and DCs). (B) Violin plots showing F2R expression across T cell subsets and GZMA expression in APCs. (C and D) Therapeutic evaluation of STNvac co-administration with F2R antagonist (F2RA, SCH79797 ) ( n = 7 mice per group). (C) Bioluminescence images showing tumor burden in orthotopic HCC-bearing mice under the indicated treatments. (D) Survival curves of mice in different groups. (E and F) Multicolor immunofluorescence staining of intratumoral <t>Ki67</t> + CD69 + ISG15 + CD8 + T cells. (E) Representative images. Scale bars, 20 μm. (F) Quantitative analysis of positive cell density in five randomly selected areas per tumor section. (G and H) Activation of human HCC TILs through the GZMA-F2R interaction. (G) Schematic illustration of the treatment schedule. (H) Quantitative analysis of 41BB + CD3 + CD8 + T cells after 24 h of GZMA stimulation ( n = 2 biological replicates, each analyzed in triplicate). Statistics: one-way ANOVA for (F) and (H); log rank (Mantel-Cox) test for (D). Mean ± SD. Significance levels: ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001. See also and .
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GZMA-F2R interaction mediates STNvac efficacy through T cell activation (A) Bubble plot showing ligand-receptor pairs between ISG15 + CD8 + T cells and APCs (B cells, CD4 + T cells, and DCs). (B) Violin plots showing F2R expression across T cell subsets and GZMA expression in APCs. (C and D) Therapeutic evaluation of STNvac co-administration with F2R antagonist (F2RA, SCH79797 ) ( n = 7 mice per group). (C) Bioluminescence images showing tumor burden in orthotopic HCC-bearing mice under the indicated treatments. (D) Survival curves of mice in different groups. (E and F) Multicolor immunofluorescence staining of intratumoral <t>Ki67</t> + CD69 + ISG15 + CD8 + T cells. (E) Representative images. Scale bars, 20 μm. (F) Quantitative analysis of positive cell density in five randomly selected areas per tumor section. (G and H) Activation of human HCC TILs through the GZMA-F2R interaction. (G) Schematic illustration of the treatment schedule. (H) Quantitative analysis of 41BB + CD3 + CD8 + T cells after 24 h of GZMA stimulation ( n = 2 biological replicates, each analyzed in triplicate). Statistics: one-way ANOVA for (F) and (H); log rank (Mantel-Cox) test for (D). Mean ± SD. Significance levels: ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001. See also and .
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In vivo anti‐endometriosis efficacy of ACS14@BSA. (A) Schematic drawing of treatment with different formulations, starting on day 3. (B) Images and (C) total volume of endometriotic lesions in mice following different treatments ( n = 8). (D) Monitoring the body weight of mice receiving different treatments ( n = 4). (E–H) RNA‐seq analysis reveals the differentially expressed genes (DEGs) in murine lesion tissues from two groups: ACS14@BSA and PBS ( n = 4). (E) Heatmap showing the significantly regulated genes identified in RNA‐seq analysis of murine ectopic lesion tissue. Gene expression values were normalized. (F) KEGG pathway enrichment analysis comparing the murine treated with ACS14@BSA to those treated with PBS. (G) Heatmap representing the genes involved in the NF‐κB signaling pathway detected in RNA‐seq analysis of murine ectopic lesion tissues. (H) Heatmap representing the genes involved in the PI3K/Akt signaling pathway detected in RNA‐seq analysis of murine ectopic lesion tissues. (I) <t>Ki67</t> staining of ectopic lesion tissues. Scale bar, 50 µm. (J) Quantification of <t>Ki67‐positive</t> cells in ectopic lesion tissues ( n = 5). (K) Fluorescence images of TUNEL staining in endometriotic lesions. Blue staining is DAPI, green staining is TUNEL. Scale bar, 50 µm. (L) Quantification of TUNEL‐positive cells in ectopic lesion tissues ( n = 5). (M) IL‐6 staining of ectopic lesion tissues. Blue staining is DAPI, green staining is IL‐6. Scale bar, 50 µm. (N) Quantification of IL‐6 mean fluorescence intensity (MFI) in ectopic lesions ( n = 6). Data are shown as the mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.
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In vivo anti‐endometriosis efficacy of ACS14@BSA. (A) Schematic drawing of treatment with different formulations, starting on day 3. (B) Images and (C) total volume of endometriotic lesions in mice following different treatments ( n = 8). (D) Monitoring the body weight of mice receiving different treatments ( n = 4). (E–H) RNA‐seq analysis reveals the differentially expressed genes (DEGs) in murine lesion tissues from two groups: ACS14@BSA and PBS ( n = 4). (E) Heatmap showing the significantly regulated genes identified in RNA‐seq analysis of murine ectopic lesion tissue. Gene expression values were normalized. (F) KEGG pathway enrichment analysis comparing the murine treated with ACS14@BSA to those treated with PBS. (G) Heatmap representing the genes involved in the NF‐κB signaling pathway detected in RNA‐seq analysis of murine ectopic lesion tissues. (H) Heatmap representing the genes involved in the PI3K/Akt signaling pathway detected in RNA‐seq analysis of murine ectopic lesion tissues. (I) <t>Ki67</t> staining of ectopic lesion tissues. Scale bar, 50 µm. (J) Quantification of <t>Ki67‐positive</t> cells in ectopic lesion tissues ( n = 5). (K) Fluorescence images of TUNEL staining in endometriotic lesions. Blue staining is DAPI, green staining is TUNEL. Scale bar, 50 µm. (L) Quantification of TUNEL‐positive cells in ectopic lesion tissues ( n = 5). (M) IL‐6 staining of ectopic lesion tissues. Blue staining is DAPI, green staining is IL‐6. Scale bar, 50 µm. (N) Quantification of IL‐6 mean fluorescence intensity (MFI) in ectopic lesions ( n = 6). Data are shown as the mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.
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In vivo anti‐endometriosis efficacy of ACS14@BSA. (A) Schematic drawing of treatment with different formulations, starting on day 3. (B) Images and (C) total volume of endometriotic lesions in mice following different treatments ( n = 8). (D) Monitoring the body weight of mice receiving different treatments ( n = 4). (E–H) RNA‐seq analysis reveals the differentially expressed genes (DEGs) in murine lesion tissues from two groups: ACS14@BSA and PBS ( n = 4). (E) Heatmap showing the significantly regulated genes identified in RNA‐seq analysis of murine ectopic lesion tissue. Gene expression values were normalized. (F) KEGG pathway enrichment analysis comparing the murine treated with ACS14@BSA to those treated with PBS. (G) Heatmap representing the genes involved in the NF‐κB signaling pathway detected in RNA‐seq analysis of murine ectopic lesion tissues. (H) Heatmap representing the genes involved in the PI3K/Akt signaling pathway detected in RNA‐seq analysis of murine ectopic lesion tissues. (I) <t>Ki67</t> staining of ectopic lesion tissues. Scale bar, 50 µm. (J) Quantification of <t>Ki67‐positive</t> cells in ectopic lesion tissues ( n = 5). (K) Fluorescence images of TUNEL staining in endometriotic lesions. Blue staining is DAPI, green staining is TUNEL. Scale bar, 50 µm. (L) Quantification of TUNEL‐positive cells in ectopic lesion tissues ( n = 5). (M) IL‐6 staining of ectopic lesion tissues. Blue staining is DAPI, green staining is IL‐6. Scale bar, 50 µm. (N) Quantification of IL‐6 mean fluorescence intensity (MFI) in ectopic lesions ( n = 6). Data are shown as the mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.
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In vivo anti‐endometriosis efficacy of ACS14@BSA. (A) Schematic drawing of treatment with different formulations, starting on day 3. (B) Images and (C) total volume of endometriotic lesions in mice following different treatments ( n = 8). (D) Monitoring the body weight of mice receiving different treatments ( n = 4). (E–H) RNA‐seq analysis reveals the differentially expressed genes (DEGs) in murine lesion tissues from two groups: ACS14@BSA and PBS ( n = 4). (E) Heatmap showing the significantly regulated genes identified in RNA‐seq analysis of murine ectopic lesion tissue. Gene expression values were normalized. (F) KEGG pathway enrichment analysis comparing the murine treated with ACS14@BSA to those treated with PBS. (G) Heatmap representing the genes involved in the NF‐κB signaling pathway detected in RNA‐seq analysis of murine ectopic lesion tissues. (H) Heatmap representing the genes involved in the PI3K/Akt signaling pathway detected in RNA‐seq analysis of murine ectopic lesion tissues. (I) <t>Ki67</t> staining of ectopic lesion tissues. Scale bar, 50 µm. (J) Quantification of <t>Ki67‐positive</t> cells in ectopic lesion tissues ( n = 5). (K) Fluorescence images of TUNEL staining in endometriotic lesions. Blue staining is DAPI, green staining is TUNEL. Scale bar, 50 µm. (L) Quantification of TUNEL‐positive cells in ectopic lesion tissues ( n = 5). (M) IL‐6 staining of ectopic lesion tissues. Blue staining is DAPI, green staining is IL‐6. Scale bar, 50 µm. (N) Quantification of IL‐6 mean fluorescence intensity (MFI) in ectopic lesions ( n = 6). Data are shown as the mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.
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In vivo anti‐endometriosis efficacy of ACS14@BSA. (A) Schematic drawing of treatment with different formulations, starting on day 3. (B) Images and (C) total volume of endometriotic lesions in mice following different treatments ( n = 8). (D) Monitoring the body weight of mice receiving different treatments ( n = 4). (E–H) RNA‐seq analysis reveals the differentially expressed genes (DEGs) in murine lesion tissues from two groups: ACS14@BSA and PBS ( n = 4). (E) Heatmap showing the significantly regulated genes identified in RNA‐seq analysis of murine ectopic lesion tissue. Gene expression values were normalized. (F) KEGG pathway enrichment analysis comparing the murine treated with ACS14@BSA to those treated with PBS. (G) Heatmap representing the genes involved in the NF‐κB signaling pathway detected in RNA‐seq analysis of murine ectopic lesion tissues. (H) Heatmap representing the genes involved in the PI3K/Akt signaling pathway detected in RNA‐seq analysis of murine ectopic lesion tissues. (I) <t>Ki67</t> staining of ectopic lesion tissues. Scale bar, 50 µm. (J) Quantification of <t>Ki67‐positive</t> cells in ectopic lesion tissues ( n = 5). (K) Fluorescence images of TUNEL staining in endometriotic lesions. Blue staining is DAPI, green staining is TUNEL. Scale bar, 50 µm. (L) Quantification of TUNEL‐positive cells in ectopic lesion tissues ( n = 5). (M) IL‐6 staining of ectopic lesion tissues. Blue staining is DAPI, green staining is IL‐6. Scale bar, 50 µm. (N) Quantification of IL‐6 mean fluorescence intensity (MFI) in ectopic lesions ( n = 6). Data are shown as the mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.
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Image Search Results


GZMA-F2R interaction mediates STNvac efficacy through T cell activation (A) Bubble plot showing ligand-receptor pairs between ISG15 + CD8 + T cells and APCs (B cells, CD4 + T cells, and DCs). (B) Violin plots showing F2R expression across T cell subsets and GZMA expression in APCs. (C and D) Therapeutic evaluation of STNvac co-administration with F2R antagonist (F2RA, SCH79797 ) ( n = 7 mice per group). (C) Bioluminescence images showing tumor burden in orthotopic HCC-bearing mice under the indicated treatments. (D) Survival curves of mice in different groups. (E and F) Multicolor immunofluorescence staining of intratumoral Ki67 + CD69 + ISG15 + CD8 + T cells. (E) Representative images. Scale bars, 20 μm. (F) Quantitative analysis of positive cell density in five randomly selected areas per tumor section. (G and H) Activation of human HCC TILs through the GZMA-F2R interaction. (G) Schematic illustration of the treatment schedule. (H) Quantitative analysis of 41BB + CD3 + CD8 + T cells after 24 h of GZMA stimulation ( n = 2 biological replicates, each analyzed in triplicate). Statistics: one-way ANOVA for (F) and (H); log rank (Mantel-Cox) test for (D). Mean ± SD. Significance levels: ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001. See also and .

Journal: Cell Reports Medicine

Article Title: Spleen-targeted neoantigen mRNA vaccine induces ISG15 + CD8 + T cell-mediated tertiary lymphoid structure formation in hepatocellular carcinoma

doi: 10.1016/j.xcrm.2026.102754

Figure Lengend Snippet: GZMA-F2R interaction mediates STNvac efficacy through T cell activation (A) Bubble plot showing ligand-receptor pairs between ISG15 + CD8 + T cells and APCs (B cells, CD4 + T cells, and DCs). (B) Violin plots showing F2R expression across T cell subsets and GZMA expression in APCs. (C and D) Therapeutic evaluation of STNvac co-administration with F2R antagonist (F2RA, SCH79797 ) ( n = 7 mice per group). (C) Bioluminescence images showing tumor burden in orthotopic HCC-bearing mice under the indicated treatments. (D) Survival curves of mice in different groups. (E and F) Multicolor immunofluorescence staining of intratumoral Ki67 + CD69 + ISG15 + CD8 + T cells. (E) Representative images. Scale bars, 20 μm. (F) Quantitative analysis of positive cell density in five randomly selected areas per tumor section. (G and H) Activation of human HCC TILs through the GZMA-F2R interaction. (G) Schematic illustration of the treatment schedule. (H) Quantitative analysis of 41BB + CD3 + CD8 + T cells after 24 h of GZMA stimulation ( n = 2 biological replicates, each analyzed in triplicate). Statistics: one-way ANOVA for (F) and (H); log rank (Mantel-Cox) test for (D). Mean ± SD. Significance levels: ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001. See also and .

Article Snippet: Ki67 immunohistochemistry (Servicebio) and TUNEL assays (One Step TUNEL Apoptosis Assay Kit, Beyotime) were conducted to evaluate tumor cell proliferation and apoptosis.

Techniques: Activation Assay, Expressing, Multicolor Immunofluorescence Staining

In vivo anti‐endometriosis efficacy of ACS14@BSA. (A) Schematic drawing of treatment with different formulations, starting on day 3. (B) Images and (C) total volume of endometriotic lesions in mice following different treatments ( n = 8). (D) Monitoring the body weight of mice receiving different treatments ( n = 4). (E–H) RNA‐seq analysis reveals the differentially expressed genes (DEGs) in murine lesion tissues from two groups: ACS14@BSA and PBS ( n = 4). (E) Heatmap showing the significantly regulated genes identified in RNA‐seq analysis of murine ectopic lesion tissue. Gene expression values were normalized. (F) KEGG pathway enrichment analysis comparing the murine treated with ACS14@BSA to those treated with PBS. (G) Heatmap representing the genes involved in the NF‐κB signaling pathway detected in RNA‐seq analysis of murine ectopic lesion tissues. (H) Heatmap representing the genes involved in the PI3K/Akt signaling pathway detected in RNA‐seq analysis of murine ectopic lesion tissues. (I) Ki67 staining of ectopic lesion tissues. Scale bar, 50 µm. (J) Quantification of Ki67‐positive cells in ectopic lesion tissues ( n = 5). (K) Fluorescence images of TUNEL staining in endometriotic lesions. Blue staining is DAPI, green staining is TUNEL. Scale bar, 50 µm. (L) Quantification of TUNEL‐positive cells in ectopic lesion tissues ( n = 5). (M) IL‐6 staining of ectopic lesion tissues. Blue staining is DAPI, green staining is IL‐6. Scale bar, 50 µm. (N) Quantification of IL‐6 mean fluorescence intensity (MFI) in ectopic lesions ( n = 6). Data are shown as the mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Advanced Science

Article Title: H 2 S‐Releasing Aspirin Nanoparticles Alleviate Endometriosis and Associated Anxiety

doi: 10.1002/advs.202520787

Figure Lengend Snippet: In vivo anti‐endometriosis efficacy of ACS14@BSA. (A) Schematic drawing of treatment with different formulations, starting on day 3. (B) Images and (C) total volume of endometriotic lesions in mice following different treatments ( n = 8). (D) Monitoring the body weight of mice receiving different treatments ( n = 4). (E–H) RNA‐seq analysis reveals the differentially expressed genes (DEGs) in murine lesion tissues from two groups: ACS14@BSA and PBS ( n = 4). (E) Heatmap showing the significantly regulated genes identified in RNA‐seq analysis of murine ectopic lesion tissue. Gene expression values were normalized. (F) KEGG pathway enrichment analysis comparing the murine treated with ACS14@BSA to those treated with PBS. (G) Heatmap representing the genes involved in the NF‐κB signaling pathway detected in RNA‐seq analysis of murine ectopic lesion tissues. (H) Heatmap representing the genes involved in the PI3K/Akt signaling pathway detected in RNA‐seq analysis of murine ectopic lesion tissues. (I) Ki67 staining of ectopic lesion tissues. Scale bar, 50 µm. (J) Quantification of Ki67‐positive cells in ectopic lesion tissues ( n = 5). (K) Fluorescence images of TUNEL staining in endometriotic lesions. Blue staining is DAPI, green staining is TUNEL. Scale bar, 50 µm. (L) Quantification of TUNEL‐positive cells in ectopic lesion tissues ( n = 5). (M) IL‐6 staining of ectopic lesion tissues. Blue staining is DAPI, green staining is IL‐6. Scale bar, 50 µm. (N) Quantification of IL‐6 mean fluorescence intensity (MFI) in ectopic lesions ( n = 6). Data are shown as the mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Immunohistochemistry for Ki67 ( GB111499 ‐100, Servicebio), immunofluorescence for IL‐6 (ab290735, abcam) and TNF‐ α (17590‐1‐AP, Proteintech), and H&E staining were performed on paraffin‐embedded mouse tissue sections.

Techniques: In Vivo, RNA Sequencing, Gene Expression, Staining, Fluorescence, TUNEL Assay