enzyme linked immunosorbent assay elisa mouse serum il 21 levels  (Multi Sciences (Lianke) Biotech Co Ltd)

Journal: Scientific Reports

Article Title: DDR2 ameliorates nonalcoholic hepatic steatosis by activating the AMPK/ACC pathway

doi: 10.1038/s41598-026-42992-0

Figure Lengend Snippet: DDR2 overexpression in hepatocytes mitigates gluconeogenesis and lipid deposition in db/db mice. ( A ) Pattern diagram of treated mice ( n = 6). ( B–C ) DDR2 mRNA ( B ) and protein ( C ) levels in the livers of db/db mice, 11 days following infection with Ad-GFP or Ad-DDR2 ( n = 6). ( D ) Representative electron microscopy images of liver sections, scale bar 1 μm; H&E-stained sections, scale bar 50 μm; Oil Red O-stained sections, scale bar 50 μm and F4/80 staining, scale bar 30 μm. ( E ) Serum glucose concentrations in 6-hour-fasted db/db mice. ( F ) Reduced serum TG induced by DDR2 overexpression. ( G ) GTT performed in Ad-GFP- or Ad-DDR2-injected db/db mice, 9 days post-injection. ( H ) PEPCK and Pgc-1α protein level in liver tissues from the two groups. ( I ) There was no significant change in TG content in the liver. ( J ) AMPK and ACC phosphorylation and Srebp-1c, Fasn and Scd-1 protein levels in liver tissue. ( K ) Reduced serum TNF-α contents following DDR2 overexpression. ( L ) eIF-2α and IRE-1α phosphorylation in mouse livers. Data are shown as mean ± SEM, with comparisons by univariate t-tests. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: Serum TNF-α levels were ascertained through an ELISA kit (E-MSEL-M0002, Elabscience Biotechnology Inc., Wuhan, China).

Techniques: Over Expression, Infection, Electron Microscopy, Staining, Injection, Phospho-proteomics

Journal: Cell Death & Disease

Article Title: CCL11 promotes hepatocellular carcinoma recurrence after surgery by potentiating immunosuppressive CCR5 + CD206 + M2-like macrophages and promoting tumor invasiveness

doi: 10.1038/s41419-026-08508-4

Figure Lengend Snippet: A Multiplexing analysis of 10 post-operative circulating cytokines in HCC patients who received liver resection. Non-Recur, non-recurrence ( N = 22); Recur, Recurrence ( N = 26). B Comparison of post-resection serum CCL11 protein between patients with and without HCC recurrence after hepatectomy. C ROC analysis of post-resection serum CCL11 protein in distinguishing patients with HCC recurrence after hepatectomy. D Kaplan-Meier analysis of post-resection serum CCL11 protein (High group vs Low group) in association with patients’ disease-free survival. E Nomogram of CCL11-integrated prediction model in predicting 5-year HCC recurrence after hepatectomy. F Comparison of ROC curves of CCL11-integrated predictive model with reference model (without CCL11) in predicting 5-year HCC recurrence after hepatectomy. G The expression level of CCL11mRNA in tumor and non-tumor liver tissues of HCC patients as well as in healthy liver tissues. H Comparison of the expression level of non-tumoral CCL11 (ntCCL11) mRNA between patients with and without HCC recurrence. I ROC curves of ntCCL11 mRNA levels in predicting 5-Year HCC recurrence after hepatectomy. J Kaplan-Meier analysis of ntCCL11 mRNA in predicting disease-free survival. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns not significant.

Article Snippet: Similarly, mouse serum CCL11 levels were measured with the Mouse CCL11/Eotaxin ELISA Kit (Proteintech).

Techniques: Multiplexing, Comparison, Expressing

Journal: Cell Death & Disease

Article Title: CCL11 promotes hepatocellular carcinoma recurrence after surgery by potentiating immunosuppressive CCR5 + CD206 + M2-like macrophages and promoting tumor invasiveness

doi: 10.1038/s41419-026-08508-4

Figure Lengend Snippet: A Correlation analyses of CCL11 levels with its receptors CCR2, CCR3 and CCR5 in non-tumoral liver tissue. B UMAP plot of CCR5+immune cells in CCL11-low group and CCL11-high group. C UMAP plot of all immune cell types. D Correlations of CCL11 levels with iNOS and CD206 in non-tumor liver tissues. E Correlation of CCL11 with CCR5 + M2-like macrophages. Kaplan-Meier survival curve of ( F ) overall survival and G disease-free survival based on CCR5 + M2-like macrophages. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Article Snippet: Similarly, mouse serum CCL11 levels were measured with the Mouse CCL11/Eotaxin ELISA Kit (Proteintech).

Techniques:

Journal: Cell Death & Disease

Article Title: CCL11 promotes hepatocellular carcinoma recurrence after surgery by potentiating immunosuppressive CCR5 + CD206 + M2-like macrophages and promoting tumor invasiveness

doi: 10.1038/s41419-026-08508-4

Figure Lengend Snippet: A Flow cytometry quantification of the number of monocyte-differentiated CCR5 + CD206 + M2-like macrophages after administration of recombinant human CCL11 (rhCCL11) protein. Control group: PBS treatment. B The expression Levels of M2-macrophage-related immunosuppressive markers and cytokines in CCL11-treated and PBS-treated CCR5 + M2-like macrophages. C Cytokine array analysis of secreted cytokines in CCL11-treated and PBS-treated CCR5 + M2-like macrophages. Red dot boxes indicate two highly upregulated cytokines: 1, MCP1; 2, IL-8. D mRNA Levels of IL-8 and MCP-1 in CCL11-treated and PBS-treated CCR5 + M2-like macrophages. E CCL11-treated CCR5 + M2-like macrophages enhanced the induction of CD4+ Foxp3+Tregs from naive CD4 + T compared to the PBS-treated control group. F Top 10 enriched KEGG pathways from differentially expressed genes in the CCL11-treated CCR5 + M2-like macrophages. G Gene set enrichment analysis of Toll-like receptor signaling pathway. H Levels of p-IKKα/β, p-IkBα, NFkB1-P50, and PD-L1 expression via western blot analysis. I Schematic diagram of the molecular mechanism of CCL11 in regulating CCR5 + M2-like macrophages. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns not significant.

Article Snippet: Similarly, mouse serum CCL11 levels were measured with the Mouse CCL11/Eotaxin ELISA Kit (Proteintech).

Techniques: Flow Cytometry, Recombinant, Control, Expressing, Western Blot

Journal: Cell Death & Disease

Article Title: CCL11 promotes hepatocellular carcinoma recurrence after surgery by potentiating immunosuppressive CCR5 + CD206 + M2-like macrophages and promoting tumor invasiveness

doi: 10.1038/s41419-026-08508-4

Figure Lengend Snippet: A Wound-healing assay to evaluate the migration of Hep3B with different concentrations of recombinant CCL11 protein (0, 12.5, 25, 50 ng/ml). B Wound-healing assay of Hep3B when blockage of CCL11-receptor CCR2, CCR3 and CCR5 in CCL11-enriched condition; C Transwell migration assay of Hep3B when blockage of CCL11-receptor CCR2, CCR3 and CCR5 in CCL11-enriched condition. D Transwell invasion assay of Hep3B when blockage of CCL11-receptor CCR2, CCR3 and CCR5 in CCL11-enriched condition. Kaplan-Meier survival curve of ( E ) Overall survival and F disease-free survival based on the expression level of CCR3 mRNA in HCC patients. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns not significant.

Article Snippet: Similarly, mouse serum CCL11 levels were measured with the Mouse CCL11/Eotaxin ELISA Kit (Proteintech).

Techniques: Wound Healing Assay, Migration, Recombinant, Transwell Migration Assay, Transwell Invasion Assay, Expressing

Journal: Cell Death & Disease

Article Title: CCL11 promotes hepatocellular carcinoma recurrence after surgery by potentiating immunosuppressive CCR5 + CD206 + M2-like macrophages and promoting tumor invasiveness

doi: 10.1038/s41419-026-08508-4

Figure Lengend Snippet: A RT2 PCR array analysis of 84 metastasis-associated genes in CCL11-treated and PBS-treated (Ctrl) HCC cells. B RT2 PCR array analysis of 84 metastasis-associated genes in CCL11 treatment (50 ng/ml) with anti-CCR3, compared to CCL11 single treatment. C Identification of upregulated genes in CCL11-high and CCR3-high in HCC from TCGA database. D Top 20 KEGG pathways associated with tumor metastasis among the 92 upregulated genes in CCL11-high & CCR3-high group. E The expression level of MMP13 mRNA CCL11-treated HCC cells followed by administration of LY294002 (PI3K inhibitor), compared with DMSO-treated control cells. F Migration assay and G Invasion assay of CCL11-treated HCC cells with or without adding LY294002. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Article Snippet: Similarly, mouse serum CCL11 levels were measured with the Mouse CCL11/Eotaxin ELISA Kit (Proteintech).

Techniques: Expressing, Control, Migration, Invasion Assay

Journal: Cell Death & Disease

Article Title: CCL11 promotes hepatocellular carcinoma recurrence after surgery by potentiating immunosuppressive CCR5 + CD206 + M2-like macrophages and promoting tumor invasiveness

doi: 10.1038/s41419-026-08508-4

Figure Lengend Snippet: A The bioinformatic analysis of MMP13-promoter binding transcript factor and AKT-activating transcript factor. B The promoter region of MMP13 gene contains 2 binding motifs for the AKT downstream transcription factor Mafk, located at nucleotide sequences -232 to -218 and -57 to -43. C Inhibition of PI3K significantly reduced the CCL11-induced Mafk transloation from cytoplasm to nuclear in HCC cells. D Western blot analysis of p-PI3K, PI3K, p-Akt, Akt, Mafk, and MMP13 protein in CCL11-treated HCC cells with and without PI3K inhibition. E Schematic diagram of mouse orthotopic HCC tumor model, followed by injection of rCCL11 Protein or PBS via portal vein. F IVIS evaluations of orthotopic HCC tumor in rCCL11 Protein group or PBS group. G Liver organs dissected from rCCL11 group or PBS group. H Western blot analysis of PI3K/Akt/MafK/MMP13 axis in rCCL11 protein group and PBS group. I Schematic diagram of the molecular mechanism of CCL11 in promoting HCC progression. *, P < 0.05; **, P < 0.01.

Article Snippet: Similarly, mouse serum CCL11 levels were measured with the Mouse CCL11/Eotaxin ELISA Kit (Proteintech).

Techniques: Binding Assay, Inhibition, Western Blot, Injection

Journal: Cell Death & Disease

Article Title: CCL11 promotes hepatocellular carcinoma recurrence after surgery by potentiating immunosuppressive CCR5 + CD206 + M2-like macrophages and promoting tumor invasiveness

doi: 10.1038/s41419-026-08508-4

Figure Lengend Snippet: A Schematic diagram of orthotopic HCC resection model, followed by anti-CCL11 therapy. B IVIS evaluations of intrahepatic and extrahepatic tumors in the control group and anti-CCL11 treatment group. C Recurred rates of recurred tumors in the control group and anti-CCL11treatment group. D Kaplan-Meier analysis for overall survival of mice after treatment. E Summary of molecular mechanisms of CCL11 in promoting HCC recurrence after liver resection. *, P < 0.05.

Article Snippet: Similarly, mouse serum CCL11 levels were measured with the Mouse CCL11/Eotaxin ELISA Kit (Proteintech).

Techniques: Control

Journal: Cells

Article Title: Cancer Immunomodulatory Effect of Bidens pilosa L. in Mice: Suppression of Tumor-Associated Macrophages and Regulatory T Cells

doi: 10.3390/cells15020126

Figure Lengend Snippet: The growth of CT26. WT syngeneic tumors in mice is inhibited by BPA . ( A ) Images of CT26. WT syngeneic tumors in mice from different treatment groups. Scale bar = 5 mm (each background grid square corresponds to 5 mm). ( B ) Tumor growth curves for syngeneic CT26.WT tumors in mice were generated from daily volume measurements during the treatment phase (n = 6). ( C ) Statistical analysis of tumor weight at the end of the study (n = 6). ( D ) Statistical analysis of serum IL-10 levels ( n = 6). ( E ) Representative immunohistochemistry (IHC) images showing the expression of the Ki67 protein in tumor tissue sections from different treatment groups. Original magnification 400×. ( F ) Quantification of Ki-67 expression in tumor tissue. The proportion of Ki-67-positive area within sections was quantified using ImageJ software and is presented as a percentage of total tissue area. Statistical significance is denoted as follows: compared to the sham group, #### p < 0.0001; Compared to the model group, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Serum IL-10 levels were detected using a mouse IL-10 ELISA Kit (Proteintech, Cat. KE10008, Wuhan, China) according to the manufacturer’s instructions.

Techniques: Generated, Immunohistochemistry, Expressing, Software