Journal: Physiological Reports

Article Title: Estrogen receptor α activation modulates the gut microbiome and type 2 diabetes risk factors

doi: 10.14814/phy2.15344

Figure Lengend Snippet: Serum hormone changes with Ex, E 2 , propylpyrazoletriyl, and diarylpropionitrile (DPN) treatment. At the end of the 10 week study, blood was collected to measure the serum adiponectin (a), resistin (b) ghrelin (c), and leptin (d) levels via an ELISA. * p < 0.05 vs. control and DPN, ** p < 0.05 vs. control and Ex, *** p < 0.05 vs. control.

Article Snippet: The serum adiponectin (22‐ADPRT‐E01, ALPCO), leptin (EZRL‐83K, Millipore), ghrelin (EZRGRT‐91K, Millipore), and resistin (32–5179; ALPCO) levels were measured via an ELISA according to the manufacturer’s instructions.

Techniques: Enzyme-linked Immunosorbent Assay, Control

Journal: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

Article Title: Resistin Enhances Monocyte Chemoattractant Protein-1 Production in Human Synovial Fibroblasts and Facilitates Monocyte Migration.

doi: 10.33594/000000029

Figure Lengend Snippet: Fig. 5. Resistin promotes MCP-1-mediated monocyte migration by inhibiting miR-33a and miR-33b. (A&B) OASFs were incubated with resistin for 24 h and miRNA expression was examined by qPCR. (C) OASFs were transfected with the miR-33a and miR-33b mimics then incubated with resistin for 24 h; MCP-1 expression was measured by qPCR. (D) CM was applied to THP-1 cells and analyzed for migration activity. Results are expressed as the mean ± SEM. *p<0.05 as compared with the control group; #p<0.05 as compared with the resistin-treated group.

Article Snippet: KG Chen et al.: Resistin Enhances MCP-1-Mediated Monocyte Migration Materials and Methods Materials Recombinant human resistin was purchased from R&D Systems (Minneapolis, MN, USA).

Techniques: Migration, Incubation, Expressing, Transfection, Activity Assay, Control

Journal: Journal of biomedical science

Article Title: Neutrophil-derived reactive agents induce a transient SpeB negative phenotype in Streptococcus pyogenes.

doi: 10.1186/s12929-023-00947-x

Figure Lengend Snippet: Fig. 1 Reversible loss of SpeB is associated with tissue pathology and inflammation. A Distribution of SpeB+ and SpeB− GAS clones directly isolated from NSTI patient tissue biopsies (n = 23). B Percentage of SpeB+ and SpeB− GAS clones after the passage in THY media (p1, passage 1; p2, passage 2). Representative analysis of 2006 GAS patient isolate is shown. C–G Correlation analysis of bacterial load (left panel; n = 81 biopsies) or percentage of SpeB− clones (right panel; n = 23 biopsies) with the presence of HMGB1 (C), IL-8 (D), infiltrating neutrophils (E), and resistin (F) in patient biopsies. Correlation was determined using Spearman test. Semiquantitative acquired computerized image analyses (ACIA) of immuno-histochemical staining were performed as described in the methods section. The cell area was defined by the hematoxylin counterstaining, and the results are presented as percent positively stained area × mean intensity of positive staining

Article Snippet: The following antibodies were used for immunohistochemistry: anti-human HMGB1 (clone EPR3507; Abcam), anti-human IL-8 (clone NAP-1; Invitrogen), anti-human resistin (clone 184,305; R&D systems), and anti-human neutrophilelastase (clone NP57; DAKO).

Techniques: Clone Assay, Isolation, Staining

Journal: Osteoarthritis and cartilage

Article Title: Resistin is elevated following traumatic joint injury and causes matrix degradation and release of inflammatory cytokines from articular cartilage in vitro.

doi: 10.1016/j.joca.2008.08.007

Figure Lengend Snippet: Fig. 2. IHC staining of synovium (A, B) and cartilage (C, D) tissues from normal (A, C) and OA (B, D) patients with an anti-resistin antibody. The arrows indicate examples of the cells positively stained with anti-resistin antibody. Magnification is 40. The images are representative of sections taken from three patients.

Article Snippet: ANTIBODY IN JOINT TISSUES Fixed, paraffin embedded synovial and cartilage tissues from three healthy and three OA patient donors were analyzed by IHC with an anti-resistin antibody (R&D Systems, Minneapolis, MN).

Techniques: Immunohistochemistry, Staining

Journal: International Journal of Molecular Sciences

Article Title: Fulvic Acid Attenuates Resistin-Induced Adhesion of HCT-116 Colorectal Cancer Cells to Endothelial Cells

doi: 10.3390/ijms161226174

Figure Lengend Snippet: Resistin induces HCT-116 and SW-48 cell adhesion to HUVECs. HCT-116 and SW-48 cells were maintained as controls or stimulated with resistin and then stained with a crystal violet solution. The adhesion of HCT-116 and SW-48 cells to HUVECs was assessed. HCT-116 and SW-48 cells incubated with resistin (50 ng/mL) plus resistin-neutralizing antibodies (Ab) exhibited no increase in HUVEC adhesion. Data represent the mean ± standard error of the mean (SEM) from four independent experiments. * p < 0.05 vs. control cells; # p < 0.05 vs. cells treated with resistin only.

Article Snippet: Recombinant human resistin was purchased from R & D Systems (Minneapolis, MN, USA).

Techniques: Staining, Incubation, Control

Journal: International Journal of Molecular Sciences

Article Title: Fulvic Acid Attenuates Resistin-Induced Adhesion of HCT-116 Colorectal Cancer Cells to Endothelial Cells

doi: 10.3390/ijms161226174

Figure Lengend Snippet: Resistin increases the expressions of ICAM-1 and VCAM-1 in HCT-116 cells. HCT-116 cells were maintained as control or stimulated with resistin. ICAM-1 and VCAM-1 mRNA ( A , B ) and protein ( C , D ) expression was analyzed. Data in ( A , B ) represent the mean ± SEM from three independent experiments. The results in ( C , D ) are representative of three independent experiments with similar results. * p < 0.05 vs. control cells.

Article Snippet: Recombinant human resistin was purchased from R & D Systems (Minneapolis, MN, USA).

Techniques: Control, Expressing

Journal: International Journal of Molecular Sciences

Article Title: Fulvic Acid Attenuates Resistin-Induced Adhesion of HCT-116 Colorectal Cancer Cells to Endothelial Cells

doi: 10.3390/ijms161226174

Figure Lengend Snippet: Blocking ICAM-1 and VCAM-1 in HCT-116 cells inhibits their adhesion to HUVECs. HCT-116 cells were pretreated with specific neutralizing antibodies ( A ) or siRNAs ( B ) for control (IgG/si-CL), ICAM-1, VCAM-1, or both and then were maintained as control or stimulated with resistin. HCT-116 cell adhesion was determined. Data represent the mean ± SEM from four independent experiments. * p < 0.05 vs. control cells (CL); # p < 0.05 vs. cells pretreated with IgG or si-CL and then treated with resistin only; ** p < 0.05 vs. cells pretreated with ICAM-1 or VCAM-1 neutralizing antibody and then treated with resistin.

Article Snippet: Recombinant human resistin was purchased from R & D Systems (Minneapolis, MN, USA).

Techniques: Blocking Assay, Control

Journal: International Journal of Molecular Sciences

Article Title: Fulvic Acid Attenuates Resistin-Induced Adhesion of HCT-116 Colorectal Cancer Cells to Endothelial Cells

doi: 10.3390/ijms161226174

Figure Lengend Snippet: Resistin-initiated HCT-116 adhesion to HUVECs is mediated by NF-κB activation. ( A ) and ( C ) HCT-116 cells were maintained as control or stimulated with resistin for 1, 2, and 4 h and then NF-κB activation ( A ) and p65 phosphorylation ( C ) were determined by ELISA kit and Western blot, respectively; ( B , D , E ) HCT-116 cells were pretreated with ( B , D ) DMSO or NF-κB inhibitors (PDTC or SN50) and ( E ) control or p65 specific siRNA and then stimulated with resistin. HCT-116 cell adhesion and ICAM-1/VCAM-1 mRNA expression were analyzed. Data represent the mean ± SEM from three independent experiments. * p < 0.05 vs. control cells; # p < 0.05 vs. DMSO or si-CL cells with resistin treatment; § p < 0.05 vs. PDTC, SN50, or si-p65 cells without resistin treatment.

Article Snippet: Recombinant human resistin was purchased from R & D Systems (Minneapolis, MN, USA).

Techniques: Activation Assay, Control, Phospho-proteomics, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing

Journal: International Journal of Molecular Sciences

Article Title: Fulvic Acid Attenuates Resistin-Induced Adhesion of HCT-116 Colorectal Cancer Cells to Endothelial Cells

doi: 10.3390/ijms161226174

Figure Lengend Snippet: FA inhibits resistin-initiated HCT-116 cell adhesion to HUVECs. ( A ) HCT-116 cells were pretreated with FA at 0, 1, 5 and 10 μg/mL and then were maintained as control or stimulated with resistin; ( B ) HCT-116 cells were pretreated with FA at 0 or 10 μg/mL and then were maintained as control or stimulated with resistin at 10, 25 and 50 ng/mL. HCT-116 cell adhesion was determined. Data represent the mean ± SEM from three independent experiments. * p < 0.05 vs. control cells; # p < 0.05 vs. cells treated with resistin only.

Article Snippet: Recombinant human resistin was purchased from R & D Systems (Minneapolis, MN, USA).

Techniques: Control

Journal: International Journal of Molecular Sciences

Article Title: Fulvic Acid Attenuates Resistin-Induced Adhesion of HCT-116 Colorectal Cancer Cells to Endothelial Cells

doi: 10.3390/ijms161226174

Figure Lengend Snippet: FA inhibits resistin-induced ICAM-1 and VCAM-1 expression in HCT-116 cells. HCT-116 cells were pretreated with FA at 0, 1, 5 and 10 μg/mL and then were maintained as control or stimulated with resistin. ICAM-1 and VCAM-1 mRNA ( A , B ) and protein ( C , D ) expression was determined. Data in ( A , B ) represent the mean ± SEM from three independent experiments. The results in ( C , D ) are representative of three independent experiments with similar results. * p < 0.05 vs. control cells; # p < 0.05 vs. cells treated with resistin only.

Article Snippet: Recombinant human resistin was purchased from R & D Systems (Minneapolis, MN, USA).

Techniques: Expressing, Control

Journal: International Journal of Molecular Sciences

Article Title: Fulvic Acid Attenuates Resistin-Induced Adhesion of HCT-116 Colorectal Cancer Cells to Endothelial Cells

doi: 10.3390/ijms161226174

Figure Lengend Snippet: FA inhibits the resistin effect on HCT-116 cell adhesion to HUVECs by down-regulating NF-κB activity. HCT-116 cells were pretreated with FA at 0, 1, 5 and 10 μg/mL and then were maintained as control or stimulated with resistin. The activation of NF-κB was determined. Data represent the mean ± SEM from three independent experiments. * p < 0.05 vs. control cells; # p < 0.05 vs. cells treated with resistin only.

Article Snippet: Recombinant human resistin was purchased from R & D Systems (Minneapolis, MN, USA).

Techniques: Activity Assay, Control, Activation Assay