s100a9 inhibitor paquinimod  (MedChemExpress)

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Neutrophil-macrophage crosstalk via NETs–IL-17/VEGF/S100A9 axis promotes hepatocellular carcinoma progression

doi: 10.1186/s13046-025-03618-x

Figure Lengend Snippet: M2 macrophage-derived VEGF induces neutrophil NETs formation by indirectly promoting HCC cell-derived S100A9. A Western blot analysis for CitH3 expression in neutrophils treated with and without CM-M0, CM-HuH-7, CM-(HuH-7 + M0), or CM-(HuH-7 + M0 + NETs) for 12 h. Densitometric values were normalized to β-actin and compared to the control group, with quantification shown in the right panel. M0 denotes THP-1-derived M0. B Representative IF images of DNA/MPO/CitH3 staining in neutrophils subjected to the same treatments as shown in A. C Western blot analysis for S100A9 expression in HuH-7 cells treated with CM-(HuH-7 + M0) or CM-(HuH-7 + M0 + NETs) for 24 h. Densitometric values were normalized to β-actin and compared to the control group, with quantification shown in the right panel. M0 denotes THP-1-derived M0. D ELISA analysis of S100A9 levels in the culture supernatant of HuH-7 cells, using the same grouping as described in C. E Western blot analysis of CitH3 expression in neutrophils following 12 h treatment with CM-(HuH-7-M0) or CM-(HuH-7-M0 + NETs), with or without Paquinimod. Densitometric values were normalized to β-actin and compared to the control group, with quantification shown in the right panel. M0 denotes THP-1-derived M0. F Representative IF images of DNA/MPO/CitH3 staining in neutrophils subjected to the same treatments as described in E. G Western blot analysis for S100A9, p-p65(S536), and p65 expression in HuH-7 cells treated with CM-(HuH-7-M0 + NETs), with or without AV-951 for 24 h. Densitometric values were normalized to β-actin and compared to the control group, with quantification presented in the right panel. M0 denotes THP-1-derived M0. H Western blot analysis of S100A9, p-p65(S536), and p65 expression in HuH-7 cells treated with or without exogenous VEGF, with or without BAY11-7082 for 24 h. Densitometric values were normalized to β-actin and compared with the control group, with quantification shown in the right panel. I Correlation analysis between serum MPO-DNA levels and NETs-IL-17 levels in HCC patients. J Correlation analysis between NETs-IL-17 levels and serum levels of VEGF in HCC patients. K Correlation analyses between serum levels of VEGF and S100A9 in HCC patients. L Correlation analyses between serum levels of S100A9 and MPO-DNA in HCC patients White scale bars: 30 μm. Data are presented as mean ± SD. Ns, not significant. * p < 0.05, ** p < 0.01, *** p < 0.001. One-way ANOVA followed by the Newman-Keuls multiple comparison test (A, C, D, E, H); Student’s t test (G)

Article Snippet: NF-κB inhibitor BAY11-7082 (10 μM; MedChemExpress, USA), S100A9 inhibitor Paquinimod (25 μM; MedChemExpress, USA), and VEGFR inhibitor AV-951 (100 nM; MedChemExpress, USA).

Techniques: Derivative Assay, Western Blot, Expressing, Control, Staining, Enzyme-linked Immunosorbent Assay, Comparison

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Neutrophil-macrophage crosstalk via NETs–IL-17/VEGF/S100A9 axis promotes hepatocellular carcinoma progression

doi: 10.1186/s13046-025-03618-x

Figure Lengend Snippet: The clinical significance of NETs-IL-17 in HCC patients. A ROC curve of serum NETs, NETs-IL-17, serum VEGF and serum S100A9 for identifying advanced stage from early stage in HCC patients. B ROC curve of serum NETs, NETs-IL-17, serum VEGF and serum S100A9 for predicting metastasis in HCC patients. C ROC curve of serum NETs, NETs-IL-17, serum VEGF and serum S100A9 for predicting extrahepatic metastasis in HCC patients. D Schematic illustration of the proposed working model: IL-17 carried by NETs activates the IL-17/NF-κB signaling pathway, promoting the polarization of M2d macrophages. These polarized M2d macrophages secrete VEGF, which stimulates HCC cells to produce S100A9. S100A9, in turn, induces neutrophils to release additional NETs, thereby establishing a positive feedback loop

Article Snippet: NF-κB inhibitor BAY11-7082 (10 μM; MedChemExpress, USA), S100A9 inhibitor Paquinimod (25 μM; MedChemExpress, USA), and VEGFR inhibitor AV-951 (100 nM; MedChemExpress, USA).

Techniques:

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

doi: 10.1016/j.jcmgh.2025.101486

Figure Lengend Snippet: The loss of FGF20 increases colonic S100A9 expression in DSS-induced mice. ( A ) Heat maps of differentially expressed proteins in the colonic tissue of FGF20 KO and WT mice with or without colitis. ( B ) Volcano diagram of proteomic analysis in FGF20 KO and WT mice with colitis. ( C ) Relative expression data of S100A9 in FGF20 KO and WT mice with or without colitis (n = 4). ( D, E ) The expression of S100A9 in the colonic tissue of each group of mice was tested by Western blot (n = 3) and immunohistochemistry (n = 4). Data are represented as mean ± SEM. Scale bar, 50 μm. ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.

Article Snippet: For the S100A9 inhibitor experiment, paquinimod (HY-100442, ABR 25757, MCE) was intraperitoneal injected to model group mice every day at a dose of 10 mg/kg, when they began to drink 2% DSS.

Techniques: Expressing, Western Blot, Immunohistochemistry

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

doi: 10.1016/j.jcmgh.2025.101486

Figure Lengend Snippet: Inhibition of S100A9 protects against colitis in FGF20 KO mice. Eight-week-old male FGF20 KO mice and WT littermates were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. In the meanwhile, paquinimod (10 mg/kg) was injected via the intraperitoneal route for 10 days. ( A, B ) Body weight and colon length of FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. ( C ) Histologic morphology of FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. Top , H&E staining; bottom , PAS staining. Scale bar, 100 μm and 50 μm. ( D ) Immunoblot analysis of colonic IL6 and iNOS in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗∗ P < .001.

Article Snippet: For the S100A9 inhibitor experiment, paquinimod (HY-100442, ABR 25757, MCE) was intraperitoneal injected to model group mice every day at a dose of 10 mg/kg, when they began to drink 2% DSS.

Techniques: Inhibition, Injection, Staining, Western Blot

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

doi: 10.1016/j.jcmgh.2025.101486

Figure Lengend Snippet: AAV-S100A9 attenuates the protective effects of FGF20-overexpression against DSS-induced colitis. Six-week-old male WT mice were treated with AAV-FGF20, AAV-S100A9, or AAV-GFP by tail vein injection. After 4 weeks of AAV injection, all mice were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. ( A ) The expression of S100A9 after AAV-S100A9 treatment was determined by Western blot (n = 6). ( B, C ) Body weights and colon length of AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not were measured. ( D ) Histologic morphology of AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not. Top , H&E staining; bottom , PAS staining. Scale bar, 100 μm and 50 μm. ( E ) Immunoblot analysis of colonic IL6 and iNOS in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.

Article Snippet: For the S100A9 inhibitor experiment, paquinimod (HY-100442, ABR 25757, MCE) was intraperitoneal injected to model group mice every day at a dose of 10 mg/kg, when they began to drink 2% DSS.

Techniques: Over Expression, Injection, Expressing, Western Blot, Staining

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

doi: 10.1016/j.jcmgh.2025.101486

Figure Lengend Snippet: Inhibition of S100A9 mitigated the deterioration of FGF20 KO on intestinal barrier function in DSS-induced colitis. Eight-week-old male FGF20 KO mice and WT littermates were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. In the meanwhile, paquinimod (10 mg/kg) was injected via the intraperitoneal route for 10 days. ( A ) Western blot and quantitation of colonic ZO-2, occludin, and claudin 1 expression in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). ( B ) Representative fluorescence images of Ki67, and the percentage of Ki67-positive cells in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. Scale bar, 50 μm (n ≥ 5). ( C ) Immunoblot analysis of colonic Bax and Bcl-2 expression in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗∗ P < .001.

Article Snippet: For the S100A9 inhibitor experiment, paquinimod (HY-100442, ABR 25757, MCE) was intraperitoneal injected to model group mice every day at a dose of 10 mg/kg, when they began to drink 2% DSS.

Techniques: Inhibition, Injection, Western Blot, Quantitation Assay, Expressing, Fluorescence

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

doi: 10.1016/j.jcmgh.2025.101486

Figure Lengend Snippet: FGF20 regulates claudin-1 through S100A9 in DSS-induced colitis mice. ( A ) Representative fluorescence images of colonic claudin-1 from FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. ( B ) Representative fluorescence images of colonic claudin-1 from AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not. Scale bar, 50 μm.

Article Snippet: For the S100A9 inhibitor experiment, paquinimod (HY-100442, ABR 25757, MCE) was intraperitoneal injected to model group mice every day at a dose of 10 mg/kg, when they began to drink 2% DSS.

Techniques: Fluorescence

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

doi: 10.1016/j.jcmgh.2025.101486

Figure Lengend Snippet: AAV-S100A9 abolished the protect effects of FGF20 overexpression on intestinal barrier function in DSS-induced colitis. Six-week-old male WT mice were treated with AAV-FGF20, AAV-S100A9, or AAV-GFP by tail vein injection. After 4 weeks of AAV injection, all mice were given 2% DSS in drinking water for 5 days, followed by normal drinking water for an additional 5 days. ( A ) Western blot and quantitation of colonic ZO-2, occludin, and claudin-1 expression in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n = 6). ( B ) Representative fluorescence images of Ki67, and the percentage of Ki67-positive cells in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n ≥ 5), Scale bar, 50 μm. ( C ) The expression of level of Bax and Bcl-2 in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not, were detected by Western blot (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001. n.s., no significance.

Article Snippet: For the S100A9 inhibitor experiment, paquinimod (HY-100442, ABR 25757, MCE) was intraperitoneal injected to model group mice every day at a dose of 10 mg/kg, when they began to drink 2% DSS.

Techniques: Over Expression, Injection, Western Blot, Quantitation Assay, Expressing, Fluorescence

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

doi: 10.1016/j.jcmgh.2025.101486

Figure Lengend Snippet: The inhibition of FGF20 on M1-like macrophage polarization in DSS-induced colitis was S100A9-dependent. ( A, B ) mRNA expression levels of macrophage M1 ( IL-6 , TNF-α , IL-1β , and MCP-1 ) and M2 ( IL-10 , Arg-1, Fizz1 , and Ym1 ) polarization-related gene in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle, were quantitatively determined by quantitative PCR (n ≥ 4). ( C, D ) mRNA expression levels of macrophage M1 ( IL-6 , TNF-α , IL-1β , and MCP-1 ) and M2 ( IL-10 , Arg-1, Fizz1 , and Ym1 ) polarization-related gene in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not, were quantitatively determined by quantitative PCR (n ≥ 4). ( E ) Representative images of immunofluorescence staining of colon sections from FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle. Scale bar, 50 μm. ( F ) Representative images of immunofluorescence staining of colon sections from AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not. Scale bar, 50 μm. Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001. n.s., no significance.

Article Snippet: For the S100A9 inhibitor experiment, paquinimod (HY-100442, ABR 25757, MCE) was intraperitoneal injected to model group mice every day at a dose of 10 mg/kg, when they began to drink 2% DSS.

Techniques: Inhibition, Expressing, Real-time Polymerase Chain Reaction, Immunofluorescence, Staining

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

doi: 10.1016/j.jcmgh.2025.101486

Figure Lengend Snippet: FGF20 inhibits NF-κB pathway through S100A9 in DDS-induced mice. ( A ) KEGG Enrichment Analysis of proteomics data from the colonic tissue of FGF20 KO and WT mice with or without colitis. ( B ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα from FGF20 KO and WT mice with or without colitis (n = 6). ( C ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα contents in AAV-FGF20- or AAV-GFP-treated mice with or without colitis. ( D ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα contents in FGF20 KO mice and WT mice with colitis, treated with paquinimod or vehicle (n = 6). ( E ) Immunoblot analysis of colonic p-P65, P65, p-IκBα, and IκBα contents in AAV-FGF20-treated mice and AAV-GFP-treated mice with colitis, treated with AAV-S100A9 or not (n = 6). Data are represented as mean ± SEM; ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.

Article Snippet: For the S100A9 inhibitor experiment, paquinimod (HY-100442, ABR 25757, MCE) was intraperitoneal injected to model group mice every day at a dose of 10 mg/kg, when they began to drink 2% DSS.

Techniques: Western Blot

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Fibroblast Growth Factor 20 Attenuates Colitis by Restoring Impaired Intestinal Epithelial Barrier Integrity and Modulating Macrophage Polarization via S100A9 in an NF-κB-Dependent Manner

doi: 10.1016/j.jcmgh.2025.101486

Figure Lengend Snippet: FGF20 inhibits M1-like macrophage polarization in NF-κB-dependent manner in vitro. Primary peritoneal macrophages were isolated from WT mice and FGF20 KO mice and used for subsequent in vitro experiments. ( A ) Immunoblot analysis of expression of iNOS, TNF-α, IL6, S100A9, p-P65, P65, p-IκBα, and IκBα in LPS-stimulated primary peritoneal macrophages, treated with or without BAY11-7082 (n = 3). ( B ) Representative immunofluorescence images and its fluorescence densities of LPS-stimulated primary peritoneal macrophages, treated with or without BAY11-7082 (n = 6). Data are represented as mean ± SEM; ∗∗ P < .01, ∗∗∗ P < .001.

Article Snippet: For the S100A9 inhibitor experiment, paquinimod (HY-100442, ABR 25757, MCE) was intraperitoneal injected to model group mice every day at a dose of 10 mg/kg, when they began to drink 2% DSS.

Techniques: In Vitro, Isolation, Western Blot, Expressing, Immunofluorescence, Fluorescence

Journal: medRxiv

Article Title: S100A9 induces neuroinflammation and aggravates early brain injury after subarachnoid hemorrhage by activating the TLR4/MYD88/NF-κB pathway

doi: 10.1101/2023.03.09.23287076

Figure Lengend Snippet: The concentration of S100A9 protein in cerebrospinal fluid (CSF) of patients with SAH, its changes with time and its correlation with short-term prognosis. A. The levels of S100A9 were detected by ELISA in CSF samples from control and patients with SAH. B. The change trend of S100A9 in CSF of patients with SAH with time. C. Horizontal box plot of S100A9 concentration in CSF and mRS at discharge in patients with SAH. *P < 0.05, ****P < 0.0001. Data were represented as the mean ± SD.

Article Snippet: Cells were treated with S100A9 inhibitors (HY-100442, Paquinimod/ABR25757, MCE, China) to mimic an in vitro knockout model. Co-cultured cells were randomly assigned into three groups: control, Hemin+Vehicle, and Hemin+Paquinimod.

Techniques: Concentration Assay, Enzyme-linked Immunosorbent Assay, Control

Journal: medRxiv

Article Title: S100A9 induces neuroinflammation and aggravates early brain injury after subarachnoid hemorrhage by activating the TLR4/MYD88/NF-κB pathway

doi: 10.1101/2023.03.09.23287076

Figure Lengend Snippet: Expression and distribution of S100A9 after SAH in mice. A-B. Representative western blotting images and quantitative analyses of S100A9 expression after SAH. n = 3 per group. ****P < 0.0001 vs Sham group; ## P < 0.01 vs SAH 24 h group. C. Representative images of double immunofluorescence staining for S100A9 in microglia, astrocytes, and neurons at 24 h after SAH. n = 3 per group. Scale bar = 50 mm. Data were represented as the mean ± SD.

Article Snippet: Cells were treated with S100A9 inhibitors (HY-100442, Paquinimod/ABR25757, MCE, China) to mimic an in vitro knockout model. Co-cultured cells were randomly assigned into three groups: control, Hemin+Vehicle, and Hemin+Paquinimod.

Techniques: Expressing, Western Blot, Double Immunofluorescence Staining

Journal: medRxiv

Article Title: S100A9 induces neuroinflammation and aggravates early brain injury after subarachnoid hemorrhage by activating the TLR4/MYD88/NF-κB pathway

doi: 10.1101/2023.03.09.23287076

Figure Lengend Snippet: S100A9 knockout can improve neurological deficit, brain edema, and reduce the damage of cortex and hippocampus after SAH 24 h. A, B. The modified Garcia and neurological score of each group. n = 10 per group. ****P < 0.0001 vs Sham group; ### P < 0.001, # P < 0.05 vs WT-SAH group. C. Quantification of brain water content. n = 3 per group. **P < 0.01 vs Sham group; # P < 0.05 vs WT-SAH group. D, E. Representative picture and quantitative analysis of western blotting from S100A9 knockout mice. n = 3 per group. ****P < 0.0001 vs WT group. F. Representative H&E staining images of brain slides. n = 3 per group. Scale bar = 50/200 µm. Data were represented as the mean ± SD.

Article Snippet: Cells were treated with S100A9 inhibitors (HY-100442, Paquinimod/ABR25757, MCE, China) to mimic an in vitro knockout model. Co-cultured cells were randomly assigned into three groups: control, Hemin+Vehicle, and Hemin+Paquinimod.

Techniques: Knock-Out, Modification, Western Blot, Staining

Journal: medRxiv

Article Title: S100A9 induces neuroinflammation and aggravates early brain injury after subarachnoid hemorrhage by activating the TLR4/MYD88/NF-κB pathway

doi: 10.1101/2023.03.09.23287076

Figure Lengend Snippet: Effect of S100A9 knockout on cortical and hippocampus neuronal injury at 72 h after SAH. A, B. The modified Garcia and neurological score of each group. n = 6 per group. ****P < 0.0001 vs Sham group; # P < 0.05 vs WT-SAH group. C, D. Representative microphotograph showed the co-localization of TUNEL positive cell (red) with NeuN (green) and quantitative analysis. n = 3 per group. ***P < 0.001 vs Sham group; # P<0.05 vs WT-SAH group. E–G. Representative picture of Nissl staining and quantitative analysis. n = 3 per group. ***P < 0.001, **P < 0.01 vs Sham group; # P < 0.05 vs WT-SAH group. Scale bar = 50 µm. Data were represented as the mean ± SD.

Article Snippet: Cells were treated with S100A9 inhibitors (HY-100442, Paquinimod/ABR25757, MCE, China) to mimic an in vitro knockout model. Co-cultured cells were randomly assigned into three groups: control, Hemin+Vehicle, and Hemin+Paquinimod.

Techniques: Knock-Out, Modification, TUNEL Assay, Staining

Journal: medRxiv

Article Title: S100A9 induces neuroinflammation and aggravates early brain injury after subarachnoid hemorrhage by activating the TLR4/MYD88/NF-κB pathway

doi: 10.1101/2023.03.09.23287076

Figure Lengend Snippet: Paquinimod can inhibit hemin-induced neuronal apoptosis. A. Representative western blotting picture of S100A9 in hemin-stimulated BV2 cells over time. B, C. CCK-8 results showed that the cell viability decreased significantly after treatment with hemin (160 mmol/L). Paquinimod (20 μmol/L) rescued the process. n = 3 per group. ***P < 0.001. D–F. Representative microphotograph showed the co-localization of TUNEL positive cell (red) with NeuN (green) and quantitative analysis. n = 3 per group. ***P < 0.001 vs control group; # P < 0.05 vs hemin+vehicle group. G, H. Representative flow cytometry images of HT22 cells, apoptotic cells represented by 7-AAD+/Annexin V+ ratio. n = 3 per group. ***P < 0.001 vs control group; ### P < 0.001 vs hemin+vehicle group. Scale bar = 50 µm. Data were represented as the mean ± SD.

Article Snippet: Cells were treated with S100A9 inhibitors (HY-100442, Paquinimod/ABR25757, MCE, China) to mimic an in vitro knockout model. Co-cultured cells were randomly assigned into three groups: control, Hemin+Vehicle, and Hemin+Paquinimod.

Techniques: Western Blot, CCK-8 Assay, TUNEL Assay, Control, Flow Cytometry

Journal: medRxiv

Article Title: S100A9 induces neuroinflammation and aggravates early brain injury after subarachnoid hemorrhage by activating the TLR4/MYD88/NF-κB pathway

doi: 10.1101/2023.03.09.23287076

Figure Lengend Snippet: S100A9 aggravates neuroinflammation after SAH. A, B. Modified Garcia and neurological scores of each group. n = 4 per group. ****P < 0.0001. **P < 0.01. *P < 0.05. C–F. Representative images and quantitative analysis of western blotting for inflammatory factors and microglial markers. n = 3 per group. ****P < 0.0001. ***P < 0.001. **P < 0.01. G, H. Representative immunofluorescence images of inflammatory factors. n = 3 per group. Scale bar = 50 µm. Data were represented as the mean ± SD.

Article Snippet: Cells were treated with S100A9 inhibitors (HY-100442, Paquinimod/ABR25757, MCE, China) to mimic an in vitro knockout model. Co-cultured cells were randomly assigned into three groups: control, Hemin+Vehicle, and Hemin+Paquinimod.

Techniques: Modification, Western Blot, Immunofluorescence

Journal: medRxiv

Article Title: S100A9 induces neuroinflammation and aggravates early brain injury after subarachnoid hemorrhage by activating the TLR4/MYD88/NF-κB pathway

doi: 10.1101/2023.03.09.23287076

Figure Lengend Snippet: S100A9 induces neuroinflammation by activating the TLR4/MYD88/NF-κB pathway. A–H. Western blotting and quantitative analyses of iNOS, TLR4, MYD88, IκBα, p-IκBα, p65, and p-p65 expression. n = 3 per group. ****P < 0.0001. ***P < 0.001. **P < 0.01. Data were represented as the mean ± SD.

Article Snippet: Cells were treated with S100A9 inhibitors (HY-100442, Paquinimod/ABR25757, MCE, China) to mimic an in vitro knockout model. Co-cultured cells were randomly assigned into three groups: control, Hemin+Vehicle, and Hemin+Paquinimod.

Techniques: Western Blot, Expressing

Journal: medRxiv

Article Title: S100A9 induces neuroinflammation and aggravates early brain injury after subarachnoid hemorrhage by activating the TLR4/MYD88/NF-κB pathway

doi: 10.1101/2023.03.09.23287076

Figure Lengend Snippet: Schematic representation of the mechanism by which S100A9 induces neuroinflammation after SAH via activation of the TLR4/MYD88/NF-κB pathway. The increased expression of S100A9 protein after SAH, activates the TLR4 receptor on microglia, and activates IκBα through MYD88 to release p65. p65 is further phosphorylated into the nucleus and binds to the effector site, inducing the M1 polarization of microglia, releasing inflammatory factors, and ultimately aggravating the early brain injury after SAH.

Article Snippet: Cells were treated with S100A9 inhibitors (HY-100442, Paquinimod/ABR25757, MCE, China) to mimic an in vitro knockout model. Co-cultured cells were randomly assigned into three groups: control, Hemin+Vehicle, and Hemin+Paquinimod.

Techniques: Activation Assay, Expressing