erk1 2 inhibitor  (MedChemExpress)

Journal: Frontiers in Immunology

Article Title: Dysregulated hyaluronan metabolism drives inflammation and angiogenesis in proliferative diabetic retinopathy

doi: 10.3389/fimmu.2026.1724199

Figure Lengend Snippet: Expression levels of hyaluronidase (Hyal)-1 (A) , CD44 (B) and receptor for hyaluronan-mediated motility (RHAMM) (C) in the retinal lysates of non-diabetic control rats (C) (n=12) and diabetic rats (D) (n=12) were determined by Western blot analysis. After determination of the intensity of the protein bands, intensities were adjusted to those of β-actin in the samples. Oxidative stress was monitored with the use of 2’,7’-Dichlorofluorescein (DCF) fluorescence intensity analysis (D) . Results are expressed as mean ± standard deviation. Ultra-Low molecular weight hyaluronan (ULMW-HA) induces breakdown of blood-retinal barrier (E) . ULMW-HA was injected intravitreally at the dose of 50 ng in 5 µL in one eye and the same volume of phosphate-buffered saline (PBS) was injected in the contralateral eye of normal rats. The BRB was quantified with the fluorescein isothiocyanate-conjugated dextran technique. Results are expressed as mean ± standard deviation of 12 rats. *p < 0.05 compared to the values obtained from PBS-injected eyes. (independent t-test). Western blot analysis of retinas demonstrated that intravitreal injection of ULMW-HA induced significant upregulation of the expression of phospho-NF-κB (F) , phospho-ERK1/2 (G) , vascular endothelial growth factor (VEGF) (H) , intercellular adhesion molecule-1 (ICAM-1) (I) , vascular cell adhesion molecule-1 (VCAM-1) (J) and high-mobility group box-1 (HMGB1) (K) . Results are expressed as mean ± standard deviation or standard error of mean of 8–10 rats in each group (*p < 0.05; independent t-test).

Article Snippet: Additionally, overnight starved Müller cells were treated with hyaluronan (ULMW-HA at 50 μg/ml, Cat No GLR003, R&D Systems) in the absence or presence of 1h pretreatment with the nuclear factor-kappa B (NF-κB) inhibitor BAY11-7085 (5 μM, Cat No sc-202490, Santa Cruz Biotechnology Inc., Santa Cruz, CA USA), or the ERK1/2 inhibitor U0126 (5 μM, Cat No sc-222395A, Santa Cruz Biotechnology Inc.) or the combination of the NF-κB inhibitor BAY11–7085 and the ERK1/2 inhibitor U0126 for 16 hours.

Techniques: Expressing, Control, Western Blot, Fluorescence, Standard Deviation, Molecular Weight, Injection, Saline

Journal: Frontiers in Immunology

Article Title: Dysregulated hyaluronan metabolism drives inflammation and angiogenesis in proliferative diabetic retinopathy

doi: 10.3389/fimmu.2026.1724199

Figure Lengend Snippet: Human retinal Müller glial cells were left untreated or treated with ultra-low molecular weight hyaluronan (ULMW-HA) (50 µg/mL) for 24 (h) (A) Protein expression of phospho-ERK1/2 and phospho-NFκB in cell lysates was determined by Western blot analysis. Levels of high mobility group box-1 (HMGB1) were quantified in the culture media by ELISA. Results are expressed as mean ± standard deviation from three different experiments each performed in triplicate (*p < 0.05; independent t-test). (B) Human retinal Müller glial cells were left untreated or treated with ULMW-HA, ULMW-HA plus BAY11-7085 (5 µM) or (C) ULMW-HA plus U-0126 (5 µM). Levels of vascular endothelial growth factor (VEGF), angiopoietin and monocyte chemotactic protein-1 (MCP-1/CCL2) were quantified in the culture media by ELISA. Results are expressed as mean ± standard deviation or standard error of mean from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three groups and two groups, respectively. *p < 0.05 compared with values obtained from untreated cells; #p < 0.05 compared with ULMW-HA plus BAY11–7085 or U-0126 treated cells. (D, E) Human retinal Müller glial cells were left untreated or treated with high glucose (HG) (25 mM), cobalt chloride (CoCl 2 ) (300 µM) or tumor necrosis factor-α (TNF-α) (5 ng/mL) with or without apigenin (10 µg/mL) for 24 (h) For HG treatment, cultures containing 25 mM mannitol were used as a control. Levels of monocyte chemotactic protein-1 (MCP-1/CCL2) (D) and vascular endothelial growth factor (VEGF) (E) were quantified in the culture media by ELISA. The results are expressed as mean ± standard deviation from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three and two groups, respectively. *p < 0.05 compared with values obtained from control cells. #p < 0.05 compared with values obtained from stimulated cells.

Article Snippet: Additionally, overnight starved Müller cells were treated with hyaluronan (ULMW-HA at 50 μg/ml, Cat No GLR003, R&D Systems) in the absence or presence of 1h pretreatment with the nuclear factor-kappa B (NF-κB) inhibitor BAY11-7085 (5 μM, Cat No sc-202490, Santa Cruz Biotechnology Inc., Santa Cruz, CA USA), or the ERK1/2 inhibitor U0126 (5 μM, Cat No sc-222395A, Santa Cruz Biotechnology Inc.) or the combination of the NF-κB inhibitor BAY11–7085 and the ERK1/2 inhibitor U0126 for 16 hours.

Techniques: Molecular Weight, Expressing, Western Blot, Enzyme-linked Immunosorbent Assay, Standard Deviation, Control

Journal: Frontiers in Immunology

Article Title: Dysregulated hyaluronan metabolism drives inflammation and angiogenesis in proliferative diabetic retinopathy

doi: 10.3389/fimmu.2026.1724199

Figure Lengend Snippet: Human retinal microvascular endothelial cells (HRMECs) were left untreated or treated with high glucose (HG) (25 mM) (A) , cobalt chloride (CoCl 2 ) (300 µM) (B) or tumor necrosis factor-α (TNF-α) (5 ng/mL) (C) with or without apigenin (10 µg/mL). For HG treatment, cultures treated with mannitol (25 mM) were used as a control. Levels of soluble syndecan-1 were quantified in the culture media by ELISA. Results are expressed as mean ± standard deviation from three different experiments each performed in triplicate. One-way ANOVA and independent t-test were used for comparisons between three and two groups, respectively. *p < 0.05 compared with values obtained from control cells. #p < 0.05 compared with values obtained from cells treated with HG, CoCl 2 or TNF-α. HRMECs were left untreated or were stimulated with ultra-low molecular weight – hyaluronan (ULMW-HA) (50 µg/mL) for 24 (h). Protein expression of phospho-ERK1/2 in the cell lysates was determined by Western blot analysis (D) . Results are expressed as mean ± standard deviation from three different experiments each performed in triplicate (*p < 0.05; independent t-test). A scratch was performed in confluent monolayers of overnight starved HRMECs with a micropipette tip subsequently, the cultures were left untreated or treated either with VEGF (10 ng/mL) or with ULMW-HA (100 µg/mL) for 16 (h) Cells were visualized using an inverted microscope. Two independent experiments were performed. Each experiment was done in duplicate, and 2–3 independent field images were taken for the migration analysis which was done by using Image J software. In the Figure, one representative image is illustrated, and the bar graphs show the analysis of all the images from each group represented as fold-change in migration versus control (E) . Results are expressed as mean ± standard deviation. One-way ANOVA and independent t-test were used for comparisons between three and two groups, respectively. *p < 0.05 compared with values obtained from control cells.

Article Snippet: Additionally, overnight starved Müller cells were treated with hyaluronan (ULMW-HA at 50 μg/ml, Cat No GLR003, R&D Systems) in the absence or presence of 1h pretreatment with the nuclear factor-kappa B (NF-κB) inhibitor BAY11-7085 (5 μM, Cat No sc-202490, Santa Cruz Biotechnology Inc., Santa Cruz, CA USA), or the ERK1/2 inhibitor U0126 (5 μM, Cat No sc-222395A, Santa Cruz Biotechnology Inc.) or the combination of the NF-κB inhibitor BAY11–7085 and the ERK1/2 inhibitor U0126 for 16 hours.

Techniques: Control, Enzyme-linked Immunosorbent Assay, Standard Deviation, Molecular Weight, Expressing, Western Blot, Inverted Microscopy, Migration, Software

Journal: Cellular & Molecular Biology Letters

Article Title: The promoting roles of GLP1R and GIPR in stemness maintenance and multiple lineage-specific differentiation of PDLSCs

doi: 10.1186/s11658-026-00867-2

Figure Lengend Snippet: Enhanced cell growth of PDLSCs facilitated by GIPRA/MAPK/ERK axis. a Western blot assay showing the expression of Ki-67, PCNA, and CCND3 affected by GIPRA as well as inhibition of cAMP/PKA/CREB, MAPK/ERK, Wnt/β-catenin, or JAK/STAT3 signaling pathways. The interpretation of bubble colors in the line chart is illustrated in Fig. a. b CCK-8 assay indicating the cell growth enhanced by GIPRA, but suppressed by ERK Inh ( n = 5 in each group). The interpretation of line colors in the line chart is illustrated in Fig. b. c Venn diagram showing the intersection of differentially binding genes by p-CREB, p-ERK1/2, TCF4, and p-STAT3 (log FC > 1, P < 0.05) compared between GIPRA and NC group. d The bubble plot displays the top ten functions of cell division and cell cycle (GO biological process) associated with the 5994 (red color highlighted) specifically binding genes by p-ERK1/2 in c . e – g IGV showing the binding peaks of p-ERK1/2 on MKI67 ( e ), PCNA ( f ), and CCND3 genes ( g ). The differential binding peaks of p-ERK1/2 on these gene promoters are highlighted by blue boxes. h – k Line plot illustrates the distribution of ChIP-seq signal intensity of p-ERK1/2 ( h ), p-CREB ( i ), TCF4 ( j ), and p-STAT3 ( k ) across the transcription start sites (±3 kb) of differentially binding genes in PDLSCs treated with GIPRA as well as GIPRA plus ERK Inh. NC, normal PDLSCs as negative control; Inh., inhibitor

Article Snippet: The in vitro treatment conditions for the small-molecule compound were as follows: GLP1RA semaglutide acetate (10 nM, 24 h), GIPRA (Pro3) GIP (0.5 nM, 24 h), GLP-1R/GIPR agonist-1 (10 nM, 24 h) also termed as 2GRA in this study, BGM0504 (2 nM, 24 h, BrightGene Pharmaceutical Co., Ltd., China) [ ], CREB inhibitor 666-15 (1 μM, 2 h, HY-101120, MCE), Akt inhibitor MK-2206 (5 μM, 24 h, HY-108232, MCE), ERK1/2 inhibitor SCH772984 (0.5 μM, 24 h, HY-50846, MCE), β-catenin inhibitor IN-3 (5 μM, 24 h, HY-147007, MCE), STAT3-IN-14 (5 μM, 2 h, HY-N10472, MCE).

Techniques: Western Blot, Expressing, Inhibition, Protein-Protein interactions, CCK-8 Assay, Binding Assay, ChIP-sequencing, Negative Control