Potential anti-inflammatory activity of 3-(4-aminophenyl) propionic acid: Effects on cell viability and nitric oxide production in synovial fibroblast (HIG-82) cells

Background Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation, the production of autoantibodies, and cartilage destruction. Synovial fibroblasts (FLS) play a central role in RA pathogenesis by secreting pro-inflammatory cytokines and invading the extracellular matrix. Objective This study evaluated the effects of 3-(4-aminophenyl)propionic acid, a propionic acid derivative nonsteroidal anti-inflammatory drug (NSAID), on cell viability and nitric oxide (NO) production in HIG-82 synovial fibroblast cells. Materials and methods Helga I. Georgescu rabbit synoviocyte cells (HIG-82) were treated with eight concentrations of 3-(4-aminophenyl)propionic acid (3.125–300 µM), with ibuprofen and diclofenac (100 µM) as controls. Cells were incubated for 24, 48, and 72 hours. Cell viability was assessed using MTT assay, and NO levels were measured with the Griess assay. Both phorbol myristate acetate (PMA)-induced and non-induced cells were studied. Results and conclusion 3-(4-aminophenyl)propionic acid exhibited no cytotoxicity across all concentrations and time points, similar to ibuprofen and diclofenac. Significant differences in cell viability between PMA-induced and non-induced groups were observed at specific concentrations (p < 0.05). Regarding NO production, the compound showed minimal inhibitory effects, while L-NAME, a nitric oxide synthase (NOS) inhibitor, strongly suppressed NO levels. The absence of PMA-induced NO in HIG-82 cells limited further assessment of the compound’s impact on NO regulation. In conclusion, 3-(4-aminophenyl)propionic acid is non-cytotoxic and maintains cell viability in synovial fibroblasts, comparable to standard NSAIDs. Although its effect on NO production could not be fully evaluated, these findings suggest its potential as a safe candidate for further anti-inflammatory studies.