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antibodies against cxcr4  (Bioss)


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    Structured Review

    Bioss antibodies against cxcr4
    Prediction of <t>CXCR4-associated</t> biological processes in the OSCC. A The differentially expressing genes in the OSCC were identified by the R software and presented as volcano plots. B The CXCR4-associated biological processes were presented by the bubble plot. CXCR4, C-X-C chemokine receptor type 4; OSCC, oral squamous cell carcinoma
    Antibodies Against Cxcr4, supplied by Bioss, used in various techniques. Bioz Stars score: 91/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against cxcr4/product/Bioss
    Average 91 stars, based on 3 article reviews
    antibodies against cxcr4 - by Bioz Stars, 2026-03
    91/100 stars

    Images

    1) Product Images from "Inhibition of CXCR4 suppresses bone invasion in a murine model of oral squamous cell carcinoma"

    Article Title: Inhibition of CXCR4 suppresses bone invasion in a murine model of oral squamous cell carcinoma

    Journal: BMC Oral Health

    doi: 10.1186/s12903-025-07544-4

    Prediction of CXCR4-associated biological processes in the OSCC. A The differentially expressing genes in the OSCC were identified by the R software and presented as volcano plots. B The CXCR4-associated biological processes were presented by the bubble plot. CXCR4, C-X-C chemokine receptor type 4; OSCC, oral squamous cell carcinoma
    Figure Legend Snippet: Prediction of CXCR4-associated biological processes in the OSCC. A The differentially expressing genes in the OSCC were identified by the R software and presented as volcano plots. B The CXCR4-associated biological processes were presented by the bubble plot. CXCR4, C-X-C chemokine receptor type 4; OSCC, oral squamous cell carcinoma

    Techniques Used: Expressing, Software

    Examination of the effect of the CXCR4 inhibitor on the bone resorption degree by HSC-3 cells in vivo. A The effect of CXCR4 inhibitor on bone resorption by HSC-3 in vivo was examined using µCT. B - H Semi-quantification of bone resorption degree according to different indicators. Data are shown as mean ± standard deviation and analyzed using the unpaired student’s t-test. * P < 0.05. CXCR4, C-X-C chemokine receptor type 4
    Figure Legend Snippet: Examination of the effect of the CXCR4 inhibitor on the bone resorption degree by HSC-3 cells in vivo. A The effect of CXCR4 inhibitor on bone resorption by HSC-3 in vivo was examined using µCT. B - H Semi-quantification of bone resorption degree according to different indicators. Data are shown as mean ± standard deviation and analyzed using the unpaired student’s t-test. * P < 0.05. CXCR4, C-X-C chemokine receptor type 4

    Techniques Used: In Vivo, Standard Deviation

    Examination of the effect of the CXCR4 inhibitor on the activation of osteoclasts in the microenvironment of HSC-3 in vivo. A H&E staining was used to present the histological findings in the different groups. B TRAP staining was used to present the TRAP-positive cells in the different groups. C Quantification of TRAP-positive cells in different groups. Black arrow indicated the TRAP-positive cells. Data are shown as mean ± standard deviation and analyzed using the unpaired student’s t-test. ** P < 0.01. CXCR4, C-X-C chemokine receptor type 4; TRAP, tartrate-resistant acid phosphatase
    Figure Legend Snippet: Examination of the effect of the CXCR4 inhibitor on the activation of osteoclasts in the microenvironment of HSC-3 in vivo. A H&E staining was used to present the histological findings in the different groups. B TRAP staining was used to present the TRAP-positive cells in the different groups. C Quantification of TRAP-positive cells in different groups. Black arrow indicated the TRAP-positive cells. Data are shown as mean ± standard deviation and analyzed using the unpaired student’s t-test. ** P < 0.01. CXCR4, C-X-C chemokine receptor type 4; TRAP, tartrate-resistant acid phosphatase

    Techniques Used: Activation Assay, In Vivo, Staining, Standard Deviation

    Examination of the effect of the CXCR4 inhibitor on the invasion and migration of HSC-3 cells in vivo. A , C , E and G Immunohistochemical staining was used to test the expression of CXCR4 ( A ), MMP9 ( C ), Snail ( E ) and vimentin ( G ) in the HSC-3 in vivo. B , D , F and H Semi-quantification of CXCR4 ( B ), MMP9 ( D ), Snail ( F ) and vimentin ( H ) expression in different groups. Data are shown as mean ± standard deviation and analyzed using the unpaired student’s t-test. * P < 0.05. CXCR4, C-X-C chemokine receptor type 4
    Figure Legend Snippet: Examination of the effect of the CXCR4 inhibitor on the invasion and migration of HSC-3 cells in vivo. A , C , E and G Immunohistochemical staining was used to test the expression of CXCR4 ( A ), MMP9 ( C ), Snail ( E ) and vimentin ( G ) in the HSC-3 in vivo. B , D , F and H Semi-quantification of CXCR4 ( B ), MMP9 ( D ), Snail ( F ) and vimentin ( H ) expression in different groups. Data are shown as mean ± standard deviation and analyzed using the unpaired student’s t-test. * P < 0.05. CXCR4, C-X-C chemokine receptor type 4

    Techniques Used: Migration, In Vivo, Immunohistochemical staining, Staining, Expressing, Standard Deviation



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    Prediction of <t>CXCR4-associated</t> biological processes in the OSCC. A The differentially expressing genes in the OSCC were identified by the R software and presented as volcano plots. B The CXCR4-associated biological processes were presented by the bubble plot. CXCR4, C-X-C chemokine receptor type 4; OSCC, oral squamous cell carcinoma
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    ALB inhibited TGF-β1-induced LX-2 cell activation via the <t>CXCL12/CXCR4</t> axis. (A) Protein expression of α-SMA and Collagen I in TGF-β1-induced LX-2 cells and treated with different concentrations of ALB. (B) Relative protein expression of α-SMA (n = 3; * P < 0.05, ** P < 0.01). (C) Relative protein expression of Collagen I (n = 3; ns, P > 0.05, * P < 0.05, ** P < 0.01). (D) KEGG enrichment analysis. (E) Heatmap analysis of gene expression profiles related to chemokine-chemokine receptor interactions in the RNA-seq dataset. (F) mRNA expression of genes related to chemokine-chemokine receptor interactions (n = 3; ns, P > 0.05, * P < 0.05, ** P < 0.01). (G) Protein expression of CXCR4 and CXCL12. (H) Relative protein expression of CXCR4 (n = 3; * P < 0.05, ** P < 0.01). (I) Relative protein expression of CXCL12 (n = 3; * P < 0.05, ** P < 0.01).
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    Figure 2. UUO induces significant upregulation of <t>CXCR4</t> and SDF-1. IHC staining was conducted to measure CXCR4 and SDF-1 expression. (A) Representative images of CXC4 and SDF-1 staining in kidneys at days seven and fourteen after UUO. Original magnification: ×200. Quantitation of CXCR4 (B) and SDF-1 (C) in mouse kidneys at days seven and fourteen after UUO in mice. Statistical analysis was performed using 1-way ANOVA followed by Tukey’s multiple comparisons test. Results are presented as mean ± SEM. ** p < 0.01. n = 6.
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    Image Search Results


    Prediction of CXCR4-associated biological processes in the OSCC. A The differentially expressing genes in the OSCC were identified by the R software and presented as volcano plots. B The CXCR4-associated biological processes were presented by the bubble plot. CXCR4, C-X-C chemokine receptor type 4; OSCC, oral squamous cell carcinoma

    Journal: BMC Oral Health

    Article Title: Inhibition of CXCR4 suppresses bone invasion in a murine model of oral squamous cell carcinoma

    doi: 10.1186/s12903-025-07544-4

    Figure Lengend Snippet: Prediction of CXCR4-associated biological processes in the OSCC. A The differentially expressing genes in the OSCC were identified by the R software and presented as volcano plots. B The CXCR4-associated biological processes were presented by the bubble plot. CXCR4, C-X-C chemokine receptor type 4; OSCC, oral squamous cell carcinoma

    Article Snippet: The sections were then incubated with primary antibodies against CXCR4 (Bioss, cat. no. bs-20317R), MMP9 (Bioss, cat. no. bs-4593R), Snail (Bioss, cat. no. bs-1371R) and Vimentin (Bioss, cat. no. bs-0756R) in 4 ̊C overnight.

    Techniques: Expressing, Software

    Examination of the effect of the CXCR4 inhibitor on the bone resorption degree by HSC-3 cells in vivo. A The effect of CXCR4 inhibitor on bone resorption by HSC-3 in vivo was examined using µCT. B - H Semi-quantification of bone resorption degree according to different indicators. Data are shown as mean ± standard deviation and analyzed using the unpaired student’s t-test. * P < 0.05. CXCR4, C-X-C chemokine receptor type 4

    Journal: BMC Oral Health

    Article Title: Inhibition of CXCR4 suppresses bone invasion in a murine model of oral squamous cell carcinoma

    doi: 10.1186/s12903-025-07544-4

    Figure Lengend Snippet: Examination of the effect of the CXCR4 inhibitor on the bone resorption degree by HSC-3 cells in vivo. A The effect of CXCR4 inhibitor on bone resorption by HSC-3 in vivo was examined using µCT. B - H Semi-quantification of bone resorption degree according to different indicators. Data are shown as mean ± standard deviation and analyzed using the unpaired student’s t-test. * P < 0.05. CXCR4, C-X-C chemokine receptor type 4

    Article Snippet: The sections were then incubated with primary antibodies against CXCR4 (Bioss, cat. no. bs-20317R), MMP9 (Bioss, cat. no. bs-4593R), Snail (Bioss, cat. no. bs-1371R) and Vimentin (Bioss, cat. no. bs-0756R) in 4 ̊C overnight.

    Techniques: In Vivo, Standard Deviation

    Examination of the effect of the CXCR4 inhibitor on the activation of osteoclasts in the microenvironment of HSC-3 in vivo. A H&E staining was used to present the histological findings in the different groups. B TRAP staining was used to present the TRAP-positive cells in the different groups. C Quantification of TRAP-positive cells in different groups. Black arrow indicated the TRAP-positive cells. Data are shown as mean ± standard deviation and analyzed using the unpaired student’s t-test. ** P < 0.01. CXCR4, C-X-C chemokine receptor type 4; TRAP, tartrate-resistant acid phosphatase

    Journal: BMC Oral Health

    Article Title: Inhibition of CXCR4 suppresses bone invasion in a murine model of oral squamous cell carcinoma

    doi: 10.1186/s12903-025-07544-4

    Figure Lengend Snippet: Examination of the effect of the CXCR4 inhibitor on the activation of osteoclasts in the microenvironment of HSC-3 in vivo. A H&E staining was used to present the histological findings in the different groups. B TRAP staining was used to present the TRAP-positive cells in the different groups. C Quantification of TRAP-positive cells in different groups. Black arrow indicated the TRAP-positive cells. Data are shown as mean ± standard deviation and analyzed using the unpaired student’s t-test. ** P < 0.01. CXCR4, C-X-C chemokine receptor type 4; TRAP, tartrate-resistant acid phosphatase

    Article Snippet: The sections were then incubated with primary antibodies against CXCR4 (Bioss, cat. no. bs-20317R), MMP9 (Bioss, cat. no. bs-4593R), Snail (Bioss, cat. no. bs-1371R) and Vimentin (Bioss, cat. no. bs-0756R) in 4 ̊C overnight.

    Techniques: Activation Assay, In Vivo, Staining, Standard Deviation

    Examination of the effect of the CXCR4 inhibitor on the invasion and migration of HSC-3 cells in vivo. A , C , E and G Immunohistochemical staining was used to test the expression of CXCR4 ( A ), MMP9 ( C ), Snail ( E ) and vimentin ( G ) in the HSC-3 in vivo. B , D , F and H Semi-quantification of CXCR4 ( B ), MMP9 ( D ), Snail ( F ) and vimentin ( H ) expression in different groups. Data are shown as mean ± standard deviation and analyzed using the unpaired student’s t-test. * P < 0.05. CXCR4, C-X-C chemokine receptor type 4

    Journal: BMC Oral Health

    Article Title: Inhibition of CXCR4 suppresses bone invasion in a murine model of oral squamous cell carcinoma

    doi: 10.1186/s12903-025-07544-4

    Figure Lengend Snippet: Examination of the effect of the CXCR4 inhibitor on the invasion and migration of HSC-3 cells in vivo. A , C , E and G Immunohistochemical staining was used to test the expression of CXCR4 ( A ), MMP9 ( C ), Snail ( E ) and vimentin ( G ) in the HSC-3 in vivo. B , D , F and H Semi-quantification of CXCR4 ( B ), MMP9 ( D ), Snail ( F ) and vimentin ( H ) expression in different groups. Data are shown as mean ± standard deviation and analyzed using the unpaired student’s t-test. * P < 0.05. CXCR4, C-X-C chemokine receptor type 4

    Article Snippet: The sections were then incubated with primary antibodies against CXCR4 (Bioss, cat. no. bs-20317R), MMP9 (Bioss, cat. no. bs-4593R), Snail (Bioss, cat. no. bs-1371R) and Vimentin (Bioss, cat. no. bs-0756R) in 4 ̊C overnight.

    Techniques: Migration, In Vivo, Immunohistochemical staining, Staining, Expressing, Standard Deviation

    ALB inhibited TGF-β1-induced LX-2 cell activation via the CXCL12/CXCR4 axis. (A) Protein expression of α-SMA and Collagen I in TGF-β1-induced LX-2 cells and treated with different concentrations of ALB. (B) Relative protein expression of α-SMA (n = 3; * P < 0.05, ** P < 0.01). (C) Relative protein expression of Collagen I (n = 3; ns, P > 0.05, * P < 0.05, ** P < 0.01). (D) KEGG enrichment analysis. (E) Heatmap analysis of gene expression profiles related to chemokine-chemokine receptor interactions in the RNA-seq dataset. (F) mRNA expression of genes related to chemokine-chemokine receptor interactions (n = 3; ns, P > 0.05, * P < 0.05, ** P < 0.01). (G) Protein expression of CXCR4 and CXCL12. (H) Relative protein expression of CXCR4 (n = 3; * P < 0.05, ** P < 0.01). (I) Relative protein expression of CXCL12 (n = 3; * P < 0.05, ** P < 0.01).

    Journal: Frontiers in Pharmacology

    Article Title: Albiflorin inhibits inflammation to improve liver fibrosis by targeting the CXCL12/CXCR4 axis in mice

    doi: 10.3389/fphar.2025.1577201

    Figure Lengend Snippet: ALB inhibited TGF-β1-induced LX-2 cell activation via the CXCL12/CXCR4 axis. (A) Protein expression of α-SMA and Collagen I in TGF-β1-induced LX-2 cells and treated with different concentrations of ALB. (B) Relative protein expression of α-SMA (n = 3; * P < 0.05, ** P < 0.01). (C) Relative protein expression of Collagen I (n = 3; ns, P > 0.05, * P < 0.05, ** P < 0.01). (D) KEGG enrichment analysis. (E) Heatmap analysis of gene expression profiles related to chemokine-chemokine receptor interactions in the RNA-seq dataset. (F) mRNA expression of genes related to chemokine-chemokine receptor interactions (n = 3; ns, P > 0.05, * P < 0.05, ** P < 0.01). (G) Protein expression of CXCR4 and CXCL12. (H) Relative protein expression of CXCR4 (n = 3; * P < 0.05, ** P < 0.01). (I) Relative protein expression of CXCL12 (n = 3; * P < 0.05, ** P < 0.01).

    Article Snippet: The antibody against CXCR4 (#60042-1-Ig) was purchased from Proteintech (Wuhan, China).

    Techniques: Activation Assay, Expressing, Gene Expression, RNA Sequencing

    ALB inhibited the activation of CXCL12/CXCR4 axis and the expression of inflammatory factors in CCl 4 -induced Mice. (A) Protein expression of CXCL12 and CXCR4. (B) Relative protein expression of CXCR4 (n = 3; * P < 0.05). (C) Relative protein expression of CXCL12 (n = 3; * P < 0.05). (D) Relative mRNA expression of CXCL12 (n = 6; * P < 0.05, ** P < 0.01). (E) Relative mRNA expression of CXCR4 (n = 6; * P < 0.05, ** P < 0.01). (F–I) Relative mRNA expression of inflammatory cytokines (n = 6; * P < 0.05).

    Journal: Frontiers in Pharmacology

    Article Title: Albiflorin inhibits inflammation to improve liver fibrosis by targeting the CXCL12/CXCR4 axis in mice

    doi: 10.3389/fphar.2025.1577201

    Figure Lengend Snippet: ALB inhibited the activation of CXCL12/CXCR4 axis and the expression of inflammatory factors in CCl 4 -induced Mice. (A) Protein expression of CXCL12 and CXCR4. (B) Relative protein expression of CXCR4 (n = 3; * P < 0.05). (C) Relative protein expression of CXCL12 (n = 3; * P < 0.05). (D) Relative mRNA expression of CXCL12 (n = 6; * P < 0.05, ** P < 0.01). (E) Relative mRNA expression of CXCR4 (n = 6; * P < 0.05, ** P < 0.01). (F–I) Relative mRNA expression of inflammatory cytokines (n = 6; * P < 0.05).

    Article Snippet: The antibody against CXCR4 (#60042-1-Ig) was purchased from Proteintech (Wuhan, China).

    Techniques: Activation Assay, Expressing

    CXCR4 inhibitor abolished the hepaprotective effect of ALB CCl 4 -induced Mice. (A) Dosing methods for the co-treatment of AMD3100 and ALB in CCl 4 -induced mouse. (B) H&E staining (bar = 50 μm), Sirius Red staining (bar = 100 μm), and Masson’s trichrome staining (bar = 100 μm) of various experimental groups. (C) Quantitative analysis of collagen fibers in Sirius Red-stained sections (n = 6; ns, P > 0.05, ** P < 0.01). (D) Quantitative analysis of collagen fibers in Masson’s trichrome-stained sections (n = 6; ns, P > 0.05, ** P < 0.01). (E) Protein expression of α-SMA and Collagen I in liver tissues of CCl 4 -induced fibrotic mice treated with AMD3100 and ALB. (F) Relative protein expression of α-SMA (n = 3; ns, P > 0.05, * P < 0.05). (G) Relative protein expression of Collagen I (n = 3; ns, P > 0.05, ** P < 0.01). (H) Protein expression of CXCL12 and CXCR4 in liver tissues of CCl 4 -induced mice treated with AMD3100 and ALB. (I) Relative protein expression of CXCL12 (n = 3; ns, P > 0.05, * P < 0.05). (J) Relative protein expression of CXCR4 (n = 3; ns, P > 0.05, * P < 0.05). (K–N) Relative mRNA expression of inflammatory cytokines (n = 6; ns, P > 0.05, * P < 0.05, ** P < 0.01).

    Journal: Frontiers in Pharmacology

    Article Title: Albiflorin inhibits inflammation to improve liver fibrosis by targeting the CXCL12/CXCR4 axis in mice

    doi: 10.3389/fphar.2025.1577201

    Figure Lengend Snippet: CXCR4 inhibitor abolished the hepaprotective effect of ALB CCl 4 -induced Mice. (A) Dosing methods for the co-treatment of AMD3100 and ALB in CCl 4 -induced mouse. (B) H&E staining (bar = 50 μm), Sirius Red staining (bar = 100 μm), and Masson’s trichrome staining (bar = 100 μm) of various experimental groups. (C) Quantitative analysis of collagen fibers in Sirius Red-stained sections (n = 6; ns, P > 0.05, ** P < 0.01). (D) Quantitative analysis of collagen fibers in Masson’s trichrome-stained sections (n = 6; ns, P > 0.05, ** P < 0.01). (E) Protein expression of α-SMA and Collagen I in liver tissues of CCl 4 -induced fibrotic mice treated with AMD3100 and ALB. (F) Relative protein expression of α-SMA (n = 3; ns, P > 0.05, * P < 0.05). (G) Relative protein expression of Collagen I (n = 3; ns, P > 0.05, ** P < 0.01). (H) Protein expression of CXCL12 and CXCR4 in liver tissues of CCl 4 -induced mice treated with AMD3100 and ALB. (I) Relative protein expression of CXCL12 (n = 3; ns, P > 0.05, * P < 0.05). (J) Relative protein expression of CXCR4 (n = 3; ns, P > 0.05, * P < 0.05). (K–N) Relative mRNA expression of inflammatory cytokines (n = 6; ns, P > 0.05, * P < 0.05, ** P < 0.01).

    Article Snippet: The antibody against CXCR4 (#60042-1-Ig) was purchased from Proteintech (Wuhan, China).

    Techniques: Staining, Expressing

    The combination of ALB and MET synergistically inhibited the progression of liver fibrosis in mice via the CXCL12/CXCR4 axis. (A) H&E staining (bar = 50 μm), Sirius Red staining (bar = 100 μm), and Masson’s trichrome staining (bar = 100 μm) of various experimental groups. (B) Quantitative analysis of collagen fibers in Sirius Red-stained sections (n = 6; ns, P > 0.05, ** P < 0.01). (C) Quantitative analysis of collagen fibers in Masson’s trichrome-stained sections (n = 6; ns, P > 0.05, ** P < 0.01). (D) Serum levels of ALT. (E) Serum levels of AST. (F) Serum levels of CRE. (G) Serum levels of BUN. (H) Protein expression of α-SMA and Collagen I in liver tissues of CCl 4 -induced mice treated with ALB and MET. (I) Relative protein expression of α-SMA (n = 3; ns, P > 0.05, * P < 0.05). (J) Relative protein expression of Collagen I (n = 3; ns, P > 0.05, ** P < 0.01). (K) Protein expression of CXCL12 and CXCR4 in liver tissues of CCl 4 -induced mice treated with ALB and MET. (L) Relative protein expression of CXCL12 (n = 3; ns, P > 0.05, * P < 0.05). (M) Relative protein expression of CXCR4 (n = 3; ns, P > 0.05, * P < 0.05).

    Journal: Frontiers in Pharmacology

    Article Title: Albiflorin inhibits inflammation to improve liver fibrosis by targeting the CXCL12/CXCR4 axis in mice

    doi: 10.3389/fphar.2025.1577201

    Figure Lengend Snippet: The combination of ALB and MET synergistically inhibited the progression of liver fibrosis in mice via the CXCL12/CXCR4 axis. (A) H&E staining (bar = 50 μm), Sirius Red staining (bar = 100 μm), and Masson’s trichrome staining (bar = 100 μm) of various experimental groups. (B) Quantitative analysis of collagen fibers in Sirius Red-stained sections (n = 6; ns, P > 0.05, ** P < 0.01). (C) Quantitative analysis of collagen fibers in Masson’s trichrome-stained sections (n = 6; ns, P > 0.05, ** P < 0.01). (D) Serum levels of ALT. (E) Serum levels of AST. (F) Serum levels of CRE. (G) Serum levels of BUN. (H) Protein expression of α-SMA and Collagen I in liver tissues of CCl 4 -induced mice treated with ALB and MET. (I) Relative protein expression of α-SMA (n = 3; ns, P > 0.05, * P < 0.05). (J) Relative protein expression of Collagen I (n = 3; ns, P > 0.05, ** P < 0.01). (K) Protein expression of CXCL12 and CXCR4 in liver tissues of CCl 4 -induced mice treated with ALB and MET. (L) Relative protein expression of CXCL12 (n = 3; ns, P > 0.05, * P < 0.05). (M) Relative protein expression of CXCR4 (n = 3; ns, P > 0.05, * P < 0.05).

    Article Snippet: The antibody against CXCR4 (#60042-1-Ig) was purchased from Proteintech (Wuhan, China).

    Techniques: Staining, Expressing

    Figure 2. UUO induces significant upregulation of CXCR4 and SDF-1. IHC staining was conducted to measure CXCR4 and SDF-1 expression. (A) Representative images of CXC4 and SDF-1 staining in kidneys at days seven and fourteen after UUO. Original magnification: ×200. Quantitation of CXCR4 (B) and SDF-1 (C) in mouse kidneys at days seven and fourteen after UUO in mice. Statistical analysis was performed using 1-way ANOVA followed by Tukey’s multiple comparisons test. Results are presented as mean ± SEM. ** p < 0.01. n = 6.

    Journal: International journal of molecular sciences

    Article Title: Second Generation I-Body AD-214 Attenuates Unilateral Ureteral Obstruction (UUO)-Induced Kidney Fibrosis Through Inhibiting Leukocyte Infiltration and Macrophage Migration.

    doi: 10.3390/ijms252313127

    Figure Lengend Snippet: Figure 2. UUO induces significant upregulation of CXCR4 and SDF-1. IHC staining was conducted to measure CXCR4 and SDF-1 expression. (A) Representative images of CXC4 and SDF-1 staining in kidneys at days seven and fourteen after UUO. Original magnification: ×200. Quantitation of CXCR4 (B) and SDF-1 (C) in mouse kidneys at days seven and fourteen after UUO in mice. Statistical analysis was performed using 1-way ANOVA followed by Tukey’s multiple comparisons test. Results are presented as mean ± SEM. ** p < 0.01. n = 6.

    Article Snippet: After preincubation with 10% protein block (Dako) to block nonspecific binding of antibodies, the tissues were incubated overnight at 4 ◦C with primary antibodies against CXCR4 (Santa Cruz, Dallas, TX, USA, sc-53534), SDF-1 (Santa Cruz, sc-74271), a-SMA (Sigma, St. Louis, MO, USA, A2547), COL-4 (Abcam, ab6586), CD11b (Abcam, ab133357), F4/80 (Abcam, ab111101), CD3 (Abcam, ab16669).

    Techniques: Immunohistochemistry, Expressing, Staining, Quantitation Assay