ro8191  (MedChemExpress)

Journal: Molecular Medicine Reports

Article Title: Fucoxanthin alleviates chondrocyte inflammation and osteoarthritis by modulating the JAK2/STAT3 signaling pathway

doi: 10.3892/mmr.2026.13933

Figure Lengend Snippet: Effects of FUC and RO8191 on cartilage degeneration and JAK2/STAT3 signaling in vivo . Representative (A) H&E-stained full-joint coronal sections and (B) corresponding high-magnification images of articular cartilage from ACLT rats treated with 200 mg/kg FUC, with or without RO8191 (n=6). Representative (C) Safranin O-Fast Green-stained full-joint coronal sections and (D) corresponding high-magnification images showing cartilage proteoglycan content (n=6). (E) OARSI scores of full-joint coronal sections, with corresponding high-magnification views (n=6). (F) Immunohistochemical staining and quantitative analysis of p-JAK2, total JAK2, p-STAT3 and total STAT3 in articular cartilage (n=6). Scale barrs: 200 µm for (A,C) full-joint coronal sections; 100 µm for (B,D) high-magnification sections. Data are presented as the mean ± SD. **P<0.01. ACLT, anterior cruciate ligament transection; FUC, fucoxanthin; OARSI, Osteoarthritis Research Society International; p, phosphorylated; JAK, Janus kinase.

Article Snippet: For the RO8191 co-treatment group, RO8191 (5 μM; cat. no. HY-W063968; MedChemExpress) was co-administered with FUC via intra-articular injections at the same volume (15 μl per joint) every 3 days for 7 weeks.

Techniques: In Vivo, Staining, Immunohistochemical staining

Journal: Molecular Medicine Reports

Article Title: Fucoxanthin alleviates chondrocyte inflammation and osteoarthritis by modulating the JAK2/STAT3 signaling pathway

doi: 10.3892/mmr.2026.13933

Figure Lengend Snippet: FUC reduces inflammatory responses associated with JAK2/STAT3 signaling in vitro . Primary rat chondrocytes were stimulated with IL-1β (10 ng/ml, 24 h) and treated with FUC (15 µM) and/or the JAK2 activator RO8191. (A) Western blot analysis and semi-quantitative evaluation of JAK2/STAT3 signaling components and inflammatory/catabolic protein expression (n=3). (B) Reverse transcription-quantitative PCR analysis of IL-6, MMP3, MMP13 and ADAMTS5 (n=3). (C) ELISA analysis of IL-6 secretion. (D) Immunofluorescence staining of MMP3 in chondrocytes with nuclei counterstained with DAPI, and corresponding quantitative fluorescence intensity analysis. Scale bar, 50 µm. Data are presented as the mean ± SD. *P<0.05; **P<0.01. NC, negative control; FUC, fucoxanthin; ADAMTS, a disintegrin and metalloproteinase with thrombospondin motifs; iNOS, inducible nitric oxide synthase; p, phosphorylated; JAK, Janus kinase.

Article Snippet: For the RO8191 co-treatment group, RO8191 (5 μM; cat. no. HY-W063968; MedChemExpress) was co-administered with FUC via intra-articular injections at the same volume (15 μl per joint) every 3 days for 7 weeks.

Techniques: In Vitro, Western Blot, Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining, Fluorescence, Negative Control

Journal: Molecular Medicine Reports

Article Title: Fucoxanthin alleviates chondrocyte inflammation and osteoarthritis by modulating the JAK2/STAT3 signaling pathway

doi: 10.3892/mmr.2026.13933

Figure Lengend Snippet: Effects of FUC and RO8191 on cartilage degeneration and JAK2/STAT3 signaling in vivo . Representative (A) H&E-stained full-joint coronal sections and (B) corresponding high-magnification images of articular cartilage from ACLT rats treated with 200 mg/kg FUC, with or without RO8191 (n=6). Representative (C) Safranin O-Fast Green-stained full-joint coronal sections and (D) corresponding high-magnification images showing cartilage proteoglycan content (n=6). (E) OARSI scores of full-joint coronal sections, with corresponding high-magnification views (n=6). (F) Immunohistochemical staining and quantitative analysis of p-JAK2, total JAK2, p-STAT3 and total STAT3 in articular cartilage (n=6). Scale barrs: 200 µm for (A,C) full-joint coronal sections; 100 µm for (B,D) high-magnification sections. Data are presented as the mean ± SD. **P<0.01. ACLT, anterior cruciate ligament transection; FUC, fucoxanthin; OARSI, Osteoarthritis Research Society International; p, phosphorylated; JAK, Janus kinase.

Article Snippet: For RO8191 treatment, chondrocytes were co-incubated with 5 μM RO8191 together with IL-1β, FUC or both at 37°C in 5% CO2 for 24 h. Recombinant rat IL-1β (cat. no. RP01788; ABclonal Biotech Co., Ltd.) was used for cell stimulation at a concentration of 10 ng/ml at 37°C for 24 h. For control groups, untreated chondrocytes served as the negative control and IL-1β-only treated chondrocytes served as the model control.

Techniques: In Vivo, Staining, Immunohistochemical staining

Journal: Molecular Medicine Reports

Article Title: Fucoxanthin alleviates chondrocyte inflammation and osteoarthritis by modulating the JAK2/STAT3 signaling pathway

doi: 10.3892/mmr.2026.13933

Figure Lengend Snippet: FUC reduces inflammatory responses associated with JAK2/STAT3 signaling in vitro . Primary rat chondrocytes were stimulated with IL-1β (10 ng/ml, 24 h) and treated with FUC (15 µM) and/or the JAK2 activator RO8191. (A) Western blot analysis and semi-quantitative evaluation of JAK2/STAT3 signaling components and inflammatory/catabolic protein expression (n=3). (B) Reverse transcription-quantitative PCR analysis of IL-6, MMP3, MMP13 and ADAMTS5 (n=3). (C) ELISA analysis of IL-6 secretion. (D) Immunofluorescence staining of MMP3 in chondrocytes with nuclei counterstained with DAPI, and corresponding quantitative fluorescence intensity analysis. Scale bar, 50 µm. Data are presented as the mean ± SD. *P<0.05; **P<0.01. NC, negative control; FUC, fucoxanthin; ADAMTS, a disintegrin and metalloproteinase with thrombospondin motifs; iNOS, inducible nitric oxide synthase; p, phosphorylated; JAK, Janus kinase.

Article Snippet: For RO8191 treatment, chondrocytes were co-incubated with 5 μM RO8191 together with IL-1β, FUC or both at 37°C in 5% CO2 for 24 h. Recombinant rat IL-1β (cat. no. RP01788; ABclonal Biotech Co., Ltd.) was used for cell stimulation at a concentration of 10 ng/ml at 37°C for 24 h. For control groups, untreated chondrocytes served as the negative control and IL-1β-only treated chondrocytes served as the model control.

Techniques: In Vitro, Western Blot, Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining, Fluorescence, Negative Control

Journal: Arteriosclerosis, Thrombosis, and Vascular Biology

Article Title: Valvular Leaflets Are Not Innocent Bystanders: Divergent Fibrotic Remodeling Accompanies Functional Mitral and Tricuspid Regurgitation

doi: 10.1161/ATVBAHA.125.324134

Figure Lengend Snippet: Elucidating the mechanism of valvular interstitial cell (VIC) subpopulation imbalance during functional tricuspid regurgitation (FTR) progression. A , Temporal differentiation trajectory curves of antifibrotic and profibrotic VIC subpopulations. B , Cell density curve plots of each antifibrotic VIC and profibrotic VIC subpopulation along pseudotime progression. C , Gene cluster heatmap and functional enrichment analysis before and after branched point 1. D , Temporal gene expression profiling of profibrotic and antifibrotic VIC markers. E , Analysis of IFN (interferon) signaling during VIC differentiation. F , Gene Set Enrichment Analysis of TGF (transforming growth factor) β signaling pathway enrichment with FTR disease severity. G , Comparison of IFITM1/3 expression between antifibrotic and profibrotic VICs (Student t test with Welch correction). H , Dot plot showing the IFN signaling intensity during the progression of FTR and functional mitral regurgitation (FMR). I , Immunofluorescence staining of IFITM1 in valve tissues from patients with different FMR stages; scale bar indicates 200 µm. J , Representative immunohistochemical images of the TGFβ signaling activation marker p-SMAD3 at different stages of FTR disease. DAPI indicates 4′,6-diamidino-2-phenylindole; DDRTree, Discriminative Dimensionality Reduction via learning a Tree; ECM, extracellular matrix; GO, gene ontology; IFN, interferon; NES, normalized enrichment score; and TV, tricuspid valve.

Article Snippet: Concurrently, RO8191, an IFN (interferon) receptor agonist (HY-W063968; MCE ), was used to examine the regulatory effects of IFN pathway activation on the phenotypic transition of valvular interstitial cells (VICs) from an antifibrotic to a profibrotic state.

Techniques: Functional Assay, Gene Expression, Comparison, Expressing, Immunofluorescence, Staining, Immunohistochemical staining, Activation Assay, Marker