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cxcl5 elisa  (Elabscience Biotechnology)


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    Elabscience Biotechnology cxcl5 elisa
    Protective effects of SMP against CCl 4 -induced acute liver injury. 8-Week-old male C57BL/6J mice were divided into the following five groups: the control group (treated daily with saline and an intraperitoneal injection of olive oil on the 14th day), CCl 4 group (treated daily with saline and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day), SMP group (treated daily with SMP at 50, 100, or 200 mg/kg, and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day). (A) Organ indices of the liver and spleen; (B) Pathological damage to the liver and spleen was assessed via H & E staining and microscopic observation. (C) The number of apoptotic cells in liver tissue was determined via TUNEL staining; (D) Cytokine levels, including those of TNF-α, CCL2, and <t>CXCL5,</t> were detected by ELISA assays; (E) Aminotransferase AST and ALT activities were detected by colorimetric assays; (F) Antioxidant indicators of the liver include SOD activity, CAT activity, and GSH content. All data are presented as the mean ± SD. Statistical significance was determined by one-way ANOVA followed by the Student–Newman–Keuls post hoc test. n = 8, *P < 0.05, **P < 0.01, ***P < 0.001.
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    Images

    1) Product Images from "Silybum marianum peptide-rich fraction alleviates acute liver injury by inhibiting TRAF3/NIK/NF-κB and is associated with changes in gut microbiota composition"

    Article Title: Silybum marianum peptide-rich fraction alleviates acute liver injury by inhibiting TRAF3/NIK/NF-κB and is associated with changes in gut microbiota composition

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2026.1915943

    Protective effects of SMP against CCl 4 -induced acute liver injury. 8-Week-old male C57BL/6J mice were divided into the following five groups: the control group (treated daily with saline and an intraperitoneal injection of olive oil on the 14th day), CCl 4 group (treated daily with saline and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day), SMP group (treated daily with SMP at 50, 100, or 200 mg/kg, and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day). (A) Organ indices of the liver and spleen; (B) Pathological damage to the liver and spleen was assessed via H & E staining and microscopic observation. (C) The number of apoptotic cells in liver tissue was determined via TUNEL staining; (D) Cytokine levels, including those of TNF-α, CCL2, and CXCL5, were detected by ELISA assays; (E) Aminotransferase AST and ALT activities were detected by colorimetric assays; (F) Antioxidant indicators of the liver include SOD activity, CAT activity, and GSH content. All data are presented as the mean ± SD. Statistical significance was determined by one-way ANOVA followed by the Student–Newman–Keuls post hoc test. n = 8, *P < 0.05, **P < 0.01, ***P < 0.001.
    Figure Legend Snippet: Protective effects of SMP against CCl 4 -induced acute liver injury. 8-Week-old male C57BL/6J mice were divided into the following five groups: the control group (treated daily with saline and an intraperitoneal injection of olive oil on the 14th day), CCl 4 group (treated daily with saline and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day), SMP group (treated daily with SMP at 50, 100, or 200 mg/kg, and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day). (A) Organ indices of the liver and spleen; (B) Pathological damage to the liver and spleen was assessed via H & E staining and microscopic observation. (C) The number of apoptotic cells in liver tissue was determined via TUNEL staining; (D) Cytokine levels, including those of TNF-α, CCL2, and CXCL5, were detected by ELISA assays; (E) Aminotransferase AST and ALT activities were detected by colorimetric assays; (F) Antioxidant indicators of the liver include SOD activity, CAT activity, and GSH content. All data are presented as the mean ± SD. Statistical significance was determined by one-way ANOVA followed by the Student–Newman–Keuls post hoc test. n = 8, *P < 0.05, **P < 0.01, ***P < 0.001.

    Techniques Used: Control, Saline, Injection, Staining, Tissue, TUNEL Assay, Enzyme-linked Immunosorbent Assay, Activity Assay

    SMP alleviated cell damage by inhibiting NIK/NF-κB. After the appropriate SMP concentration (0, 0.01, 0.1, 1, 10, 20, 40, 80, or 160 μg/mL) was determined in normal Hepa1-6 cells, the effect of SMP on the expression of inflammation-induced marker genes was evaluated in Hepa1-6 cells overexpressing the NIK gene. Hepa1-6 cells were divided into the following five groups (n = 3): the oe-vector group (overexpressing vector and administered saline), the solvent group (overexpressing the NIK gene and administered solvent), and the SMP group (overexpressing the NIK gene and administered SMP at concentrations of 10, 20, or 40 μg/mL). (A) CCK8 assay was used to measure the viability of normal Hepa1-6 cells; (B) Protein expression levels of NRF2, NIK, and p52 determined via Western blot; (C) Relative dual luciferase activity indicating transcription activity; (D) mRNA expression levels of TNF-α, CCL2, and CCL5, as detected by qPCR; (E) Cytokine levels, including those of TNF-α, CCL2, and CCL5, were detected via ELISA; (F) The mRNA expression levels of CXCL5 and NOS2 were detected by qPCR. Data are presented as the mean ± SD from three independent experiments (n = 3), with three technical replicates per independent experiment. Statistical significance was determined by one-way ANOVA followed by the Student–Newman–Keuls post hoc test. N = 3, *P < 0.05, **P < 0.01, ***P < 0.001. SMP, Silybum marianum peptides.
    Figure Legend Snippet: SMP alleviated cell damage by inhibiting NIK/NF-κB. After the appropriate SMP concentration (0, 0.01, 0.1, 1, 10, 20, 40, 80, or 160 μg/mL) was determined in normal Hepa1-6 cells, the effect of SMP on the expression of inflammation-induced marker genes was evaluated in Hepa1-6 cells overexpressing the NIK gene. Hepa1-6 cells were divided into the following five groups (n = 3): the oe-vector group (overexpressing vector and administered saline), the solvent group (overexpressing the NIK gene and administered solvent), and the SMP group (overexpressing the NIK gene and administered SMP at concentrations of 10, 20, or 40 μg/mL). (A) CCK8 assay was used to measure the viability of normal Hepa1-6 cells; (B) Protein expression levels of NRF2, NIK, and p52 determined via Western blot; (C) Relative dual luciferase activity indicating transcription activity; (D) mRNA expression levels of TNF-α, CCL2, and CCL5, as detected by qPCR; (E) Cytokine levels, including those of TNF-α, CCL2, and CCL5, were detected via ELISA; (F) The mRNA expression levels of CXCL5 and NOS2 were detected by qPCR. Data are presented as the mean ± SD from three independent experiments (n = 3), with three technical replicates per independent experiment. Statistical significance was determined by one-way ANOVA followed by the Student–Newman–Keuls post hoc test. N = 3, *P < 0.05, **P < 0.01, ***P < 0.001. SMP, Silybum marianum peptides.

    Techniques Used: Concentration Assay, Expressing, Marker, Plasmid Preparation, Saline, Solvent, CCK-8 Assay, Western Blot, Luciferase, Activity Assay, Enzyme-linked Immunosorbent Assay


    Figure Legend Snippet:

    Techniques Used:

    Related Articles

    Enzyme-linked Immunosorbent Assay:

    Article Title: Tumor-derived CCL15 regulates RNA m 6 A methylation in cancer-associated fibroblasts to promote hepatocellular carcinoma growth.
    Article Snippet: Hepatocellular carcinoma (HCC) is a lethal malignancy characterized by rapid growth.. The interaction between tumor cells and cancer-associated fibroblasts (CAFs) significantly influences HCC progression.. CCL15, a CC chemokine family member, is predominantly expressed in HCC and strongly correlates with tumor size, indicating its critical role in HCC growth.

    Article Title: ZFP36L1 promotes non-small cell lung cancer progression under hypoxia by modulating CXCL9:SPP1 polarity: A single-cell transcriptomic study.
    Article Snippet: Reaction was stopped by 50 μL of stop solution beforemeasuring optical density (OD; 450 nm) on amicroplate reader (Bio-Rad). .. CXCL10 (mouse: E-EL-M0021; human: E-ELH0050), IL-1β (mouse: E-EL-M0037; human: E-EL-H0149) and CXCL5 (mouse: E-EL-M0471; human: E-EL-H0046) ELISA kits from Elabscience (China) and IL-7 ELISA kits (mouse: EMIL7; human: EHIL7) fromThermoFisherwere used. ..

    Cell Culture:

    Article Title: Tumor-derived CCL15 regulates RNA m 6 A methylation in cancer-associated fibroblasts to promote hepatocellular carcinoma growth.
    Article Snippet: Hepatocellular carcinoma (HCC) is a lethal malignancy characterized by rapid growth.. The interaction between tumor cells and cancer-associated fibroblasts (CAFs) significantly influences HCC progression.. CCL15, a CC chemokine family member, is predominantly expressed in HCC and strongly correlates with tumor size, indicating its critical role in HCC growth.



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    Protective effects of SMP against CCl 4 -induced acute liver injury. 8-Week-old male C57BL/6J mice were divided into the following five groups: the control group (treated daily with saline and an intraperitoneal injection of olive oil on the 14th day), CCl 4 group (treated daily with saline and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day), SMP group (treated daily with SMP at 50, 100, or 200 mg/kg, and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day). (A) Organ indices of the liver and spleen; (B) Pathological damage to the liver and spleen was assessed via H & E staining and microscopic observation. (C) The number of apoptotic cells in liver tissue was determined via TUNEL staining; (D) Cytokine levels, including those of TNF-α, CCL2, and CXCL5, were detected by ELISA assays; (E) Aminotransferase AST and ALT activities were detected by colorimetric assays; (F) Antioxidant indicators of the liver include SOD activity, CAT activity, and GSH content. All data are presented as the mean ± SD. Statistical significance was determined by one-way ANOVA followed by the Student–Newman–Keuls post hoc test. n = 8, *P < 0.05, **P < 0.01, ***P < 0.001.

    Journal: Frontiers in Pharmacology

    Article Title: Silybum marianum peptide-rich fraction alleviates acute liver injury by inhibiting TRAF3/NIK/NF-κB and is associated with changes in gut microbiota composition

    doi: 10.3389/fphar.2026.1915943

    Figure Lengend Snippet: Protective effects of SMP against CCl 4 -induced acute liver injury. 8-Week-old male C57BL/6J mice were divided into the following five groups: the control group (treated daily with saline and an intraperitoneal injection of olive oil on the 14th day), CCl 4 group (treated daily with saline and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day), SMP group (treated daily with SMP at 50, 100, or 200 mg/kg, and an intraperitoneal injection of CCl 4 dissolved in olive oil on the 14th day). (A) Organ indices of the liver and spleen; (B) Pathological damage to the liver and spleen was assessed via H & E staining and microscopic observation. (C) The number of apoptotic cells in liver tissue was determined via TUNEL staining; (D) Cytokine levels, including those of TNF-α, CCL2, and CXCL5, were detected by ELISA assays; (E) Aminotransferase AST and ALT activities were detected by colorimetric assays; (F) Antioxidant indicators of the liver include SOD activity, CAT activity, and GSH content. All data are presented as the mean ± SD. Statistical significance was determined by one-way ANOVA followed by the Student–Newman–Keuls post hoc test. n = 8, *P < 0.05, **P < 0.01, ***P < 0.001.

    Article Snippet: The mouse serum prepared from each group was subjected to TNF-α, CCL2, and CXCL5 ELISA (Elabscience).

    Techniques: Control, Saline, Injection, Staining, Tissue, TUNEL Assay, Enzyme-linked Immunosorbent Assay, Activity Assay

    SMP alleviated cell damage by inhibiting NIK/NF-κB. After the appropriate SMP concentration (0, 0.01, 0.1, 1, 10, 20, 40, 80, or 160 μg/mL) was determined in normal Hepa1-6 cells, the effect of SMP on the expression of inflammation-induced marker genes was evaluated in Hepa1-6 cells overexpressing the NIK gene. Hepa1-6 cells were divided into the following five groups (n = 3): the oe-vector group (overexpressing vector and administered saline), the solvent group (overexpressing the NIK gene and administered solvent), and the SMP group (overexpressing the NIK gene and administered SMP at concentrations of 10, 20, or 40 μg/mL). (A) CCK8 assay was used to measure the viability of normal Hepa1-6 cells; (B) Protein expression levels of NRF2, NIK, and p52 determined via Western blot; (C) Relative dual luciferase activity indicating transcription activity; (D) mRNA expression levels of TNF-α, CCL2, and CCL5, as detected by qPCR; (E) Cytokine levels, including those of TNF-α, CCL2, and CCL5, were detected via ELISA; (F) The mRNA expression levels of CXCL5 and NOS2 were detected by qPCR. Data are presented as the mean ± SD from three independent experiments (n = 3), with three technical replicates per independent experiment. Statistical significance was determined by one-way ANOVA followed by the Student–Newman–Keuls post hoc test. N = 3, *P < 0.05, **P < 0.01, ***P < 0.001. SMP, Silybum marianum peptides.

    Journal: Frontiers in Pharmacology

    Article Title: Silybum marianum peptide-rich fraction alleviates acute liver injury by inhibiting TRAF3/NIK/NF-κB and is associated with changes in gut microbiota composition

    doi: 10.3389/fphar.2026.1915943

    Figure Lengend Snippet: SMP alleviated cell damage by inhibiting NIK/NF-κB. After the appropriate SMP concentration (0, 0.01, 0.1, 1, 10, 20, 40, 80, or 160 μg/mL) was determined in normal Hepa1-6 cells, the effect of SMP on the expression of inflammation-induced marker genes was evaluated in Hepa1-6 cells overexpressing the NIK gene. Hepa1-6 cells were divided into the following five groups (n = 3): the oe-vector group (overexpressing vector and administered saline), the solvent group (overexpressing the NIK gene and administered solvent), and the SMP group (overexpressing the NIK gene and administered SMP at concentrations of 10, 20, or 40 μg/mL). (A) CCK8 assay was used to measure the viability of normal Hepa1-6 cells; (B) Protein expression levels of NRF2, NIK, and p52 determined via Western blot; (C) Relative dual luciferase activity indicating transcription activity; (D) mRNA expression levels of TNF-α, CCL2, and CCL5, as detected by qPCR; (E) Cytokine levels, including those of TNF-α, CCL2, and CCL5, were detected via ELISA; (F) The mRNA expression levels of CXCL5 and NOS2 were detected by qPCR. Data are presented as the mean ± SD from three independent experiments (n = 3), with three technical replicates per independent experiment. Statistical significance was determined by one-way ANOVA followed by the Student–Newman–Keuls post hoc test. N = 3, *P < 0.05, **P < 0.01, ***P < 0.001. SMP, Silybum marianum peptides.

    Article Snippet: The mouse serum prepared from each group was subjected to TNF-α, CCL2, and CXCL5 ELISA (Elabscience).

    Techniques: Concentration Assay, Expressing, Marker, Plasmid Preparation, Saline, Solvent, CCK-8 Assay, Western Blot, Luciferase, Activity Assay, Enzyme-linked Immunosorbent Assay

    Journal: Frontiers in Pharmacology

    Article Title: Silybum marianum peptide-rich fraction alleviates acute liver injury by inhibiting TRAF3/NIK/NF-κB and is associated with changes in gut microbiota composition

    doi: 10.3389/fphar.2026.1915943

    Figure Lengend Snippet:

    Article Snippet: The mouse serum prepared from each group was subjected to TNF-α, CCL2, and CXCL5 ELISA (Elabscience).

    Techniques:

    Distinct immune microenvironment across LIHV-defined subgroups (A) Immune cell abundance comparison across subgroups using the indicated immune analysis tools across four independent iCCA cohorts. Circle color and size represent log 2 fold change and p value, respectively. (B) Boxplots of CD66b + neutrophils, CD68 + macrophages, CD3 + T cells, CD20 + B cells, and αSMA + fibroblasts across subgroups (Mann-Whitney U test). (C) Heatmap of immune signatures and checkpoint expression summarized as mean Z scores per subgroup across four cohorts. ∗FDR < 0.05; ∗∗FDR < 0.01; ∗∗∗FDR < 0.001. (D) Heatmap of Spearman correlations between chemokine expression and neutrophil infiltration. IHC, immunohistochemistry. (E) Boxplot comparing CXCL5 expression across subgroups in the Fu-iCCA cohort (Mann-Whitney U test). (F) Dot heatmap of chemokine gene expression across major cell types in Xue’s scRNA-seq dataset. (G) Boxplots of average CXCL5 expression in tumor cells and macrophages across subgroups (Mann-Whitney U test). (H) Western blot validating CXCL5 knockdown and overexpression efficiency in RBE and HuCCT1 cells. (I) Quantification of migrated neutrophils in transwell assays co-cultured with modified RBE and HuCCT1 cells ( n = 4 replicates per group; mean ± SD; Student’s t test). (J) Western blot analysis of CXCL5 overexpression in KTP cells. (K) Tumor growth curves of mice injected with control or CXCL5-overexpressing KTP cells ( n = 6 per group; mean ± SEM; Student’s t test). (L) Proportion and number of infiltrated neutrophils in control and CXCL5-overexpressing KTP tumors ( n = 6 per group; Student’s t test). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. See also and and .

    Journal: Cell Reports Medicine

    Article Title: Robust transcriptomic hallmarks targeting intratumor heterogeneity in intrahepatic cholangiocarcinoma

    doi: 10.1016/j.xcrm.2026.102708

    Figure Lengend Snippet: Distinct immune microenvironment across LIHV-defined subgroups (A) Immune cell abundance comparison across subgroups using the indicated immune analysis tools across four independent iCCA cohorts. Circle color and size represent log 2 fold change and p value, respectively. (B) Boxplots of CD66b + neutrophils, CD68 + macrophages, CD3 + T cells, CD20 + B cells, and αSMA + fibroblasts across subgroups (Mann-Whitney U test). (C) Heatmap of immune signatures and checkpoint expression summarized as mean Z scores per subgroup across four cohorts. ∗FDR < 0.05; ∗∗FDR < 0.01; ∗∗∗FDR < 0.001. (D) Heatmap of Spearman correlations between chemokine expression and neutrophil infiltration. IHC, immunohistochemistry. (E) Boxplot comparing CXCL5 expression across subgroups in the Fu-iCCA cohort (Mann-Whitney U test). (F) Dot heatmap of chemokine gene expression across major cell types in Xue’s scRNA-seq dataset. (G) Boxplots of average CXCL5 expression in tumor cells and macrophages across subgroups (Mann-Whitney U test). (H) Western blot validating CXCL5 knockdown and overexpression efficiency in RBE and HuCCT1 cells. (I) Quantification of migrated neutrophils in transwell assays co-cultured with modified RBE and HuCCT1 cells ( n = 4 replicates per group; mean ± SD; Student’s t test). (J) Western blot analysis of CXCL5 overexpression in KTP cells. (K) Tumor growth curves of mice injected with control or CXCL5-overexpressing KTP cells ( n = 6 per group; mean ± SEM; Student’s t test). (L) Proportion and number of infiltrated neutrophils in control and CXCL5-overexpressing KTP tumors ( n = 6 per group; Student’s t test). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. See also and and .

    Article Snippet: A CXCL5 neutralizing antibody (R&D Systems, AF254) was added at 5 μg/mL.

    Techniques: Comparison, MANN-WHITNEY, Expressing, Immunohistochemistry, Gene Expression, Western Blot, Knockdown, Over Expression, Cell Culture, Modification, Injection, Control