Journal: Frontiers in Pharmacology

Article Title: Ranitidine attenuates myocardial fibrosis by suppressing histamine/H2 receptor signaling and FAK/Src activation

doi: 10.3389/fphar.2026.1874499

Figure Lengend Snippet: Ranitidine inhibits TGF-β1-induced total collagen accumulation in NIH/3T3 fibroblasts. Total collagen content was measured by Sirius red assay. Data are presented as mean ± SD from three independent experiments. *p < 0.05.

Article Snippet: Key reagents included ranitidine (Macklin, R838252, purity >98%), valsartan (Macklin, V844023, purity >95%), and TGF-β1 (MedChemExpress, HY-P7117, purity >95%).

Techniques:

Journal: Frontiers in Pharmacology

Article Title: Ranitidine attenuates myocardial fibrosis by suppressing histamine/H2 receptor signaling and FAK/Src activation

doi: 10.3389/fphar.2026.1874499

Figure Lengend Snippet: Ranitidine inhibits the expression of fibrosis-related proteins and reduces FAK/Src activation in TGF-β1-stimulated fibroblasts. (A) Representative Western blot images of p-FAK, FAK, p-Src, Src, α-SMA, Collagen I, Collagen III, and GAPDH in fibroblasts treated with TGF-β1 (15 ng/mL) with or without ranitidine (RN, 0.1, 1, and 10 μM). (B–D) Quantification of α-SMA, Collagen I, and Collagen III protein expression. (E,F) Quantification of p-FAK and p-Src protein expression. Data are presented as mean ± SD from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Article Snippet: Key reagents included ranitidine (Macklin, R838252, purity >98%), valsartan (Macklin, V844023, purity >95%), and TGF-β1 (MedChemExpress, HY-P7117, purity >95%).

Techniques: Expressing, Activation Assay, Western Blot

Journal: Frontiers in Pharmacology

Article Title: Ranitidine attenuates myocardial fibrosis by suppressing histamine/H2 receptor signaling and FAK/Src activation

doi: 10.3389/fphar.2026.1874499

Figure Lengend Snippet: Ranitidine reduces the mRNA expression of fibrosis-related markers in TGF-β1-stimulated fibroblasts. (A–C) Relative mRNA expression levels of α-SMA, Collagen I, and Collagen III in fibroblasts treated with TGF-β1 (15 ng/mL) with or without ranitidine (RN, 0.1, 1, and 10 μM). Data are presented as mean ± SD from three independent experiments. ***p < 0.001.

Article Snippet: Key reagents included ranitidine (Macklin, R838252, purity >98%), valsartan (Macklin, V844023, purity >95%), and TGF-β1 (MedChemExpress, HY-P7117, purity >95%).

Techniques: Expressing

Journal: Neural Regeneration Research

Article Title: Small extracellular vesicles derived from hair follicle neural crest stem cells enhance perineurial cell proliferation and migration via the TGF-β/SMAD/HAS2 pathway

doi: 10.4103/NRR.NRR-D-25-00127

Figure Lengend Snippet: miR-21-5p activates the TGF-β/SMAD pathway by inhibiting SMAD7, resulting in upregulated HAS2 and increased PC proliferation and migration. (A, B) The volcano plot (A) and heatmap (B) illustrated the differential gene expression in regenerated tissue between the phosphate-buffered saline (PBS) and small extracellular vesicles derived from hair follicle neural crest stem cells (hfNCSC-sEVs) groups on day 7 post-operation ( n = 3 per group). (C) The chord diagram of the Gene Ontology enrichment analysis and (D) bubble chart of the Kyoto Encyclopedia of Genes and Genomes enrichment analysis for differential genes highlighted the enriched functions and associated pathways. (E) The pie chart displayed the top 10 most abundant microRNAs (miRNAs) in hfNCSC-sEVs. (F) Schematic representation of the predicted binding sites of miR-21-5p on its target gene Smad7 , as identified by TargetScan. (G) Quantitative reverse transcription-polymerase chain reaction results indicated the relative expression levels of miR-21-5p in PCs from the PBS and hfNCSC-sEVs groups on day 3 of in vitro culture ( n = 3 per group). (H) The dual-luciferase reporter assay demonstrated the relative luciferase activity following the co-transfection of reporter constructs from the Control, wild-type (WT) Smad7 3′ untranslated region (UTR), and mutant Smad7 3′ UTR groups with either miR-21-5p overexpression plasmid or negative control vector ( n = 3 per group). (I, J) Western blot (I) and statistical analysis (J) revealed the relative protein expression levels of SMAD7 and HAS2, as well as the phosphorylation levels of SMAD2/3 in PCs from the –/–, TGF-β/–, and TGF-β/miR-21-5p groups on day 5 of in vitro culture (normalized to β-actin, n = 3 per group). Data are expressed as the mean ± SEM. ** P < 0.01, *** P < 0.001 (Student’s t -test for G; one-way analysis of variance and Tukey’s multiple comparison test for J, H). The data were from at least three separate and independent studies. GO: Gene Ontology; HAS2: hyaluronan synthase 2; hfNCSCs: hair follicle neural crest stem cells; KEGG: Kyoto Encyclopedia of Genes and Genomes; MUT: mutant; NC: negative control; ns: not significant; PCs: perineurial cells; sEVs: small extracellular vesicles; SMAD: mothers against decapentaplegic homolog; TGF-β: transforming growth factor-beta; WT: wild type.

Article Snippet: For cell treatment, transforming growth factor (TGF)-β (Cat# HY- P70648 , MedChemExpress, Monmouth Junction, NJ, USA) was administered at a concentration of 5 ng/mL. miR-21-5p mimics or si- Has2 , provided by Sangon Biotech Co., Ltd., were transfected using Lipofectamine RNAiMAX reagent (Cat# L13778150, Invitrogen) according to the instructions.

Techniques: Migration, Gene Expression, Saline, Derivative Assay, Binding Assay, Reverse Transcription, Polymerase Chain Reaction, Expressing, In Vitro, Luciferase, Reporter Assay, Activity Assay, Cotransfection, Construct, Control, Mutagenesis, Over Expression, Plasmid Preparation, Negative Control, Western Blot, Phospho-proteomics, Comparison