Activin regulates inflammation, cell proliferation, immune response, wound repair, and endocrine function. In this study, we investigated the effect of activin on inflammatory genes in THP-1 cells and the involvement of NF-KB, AKT, and mitogen-activated protein kinase (MAPK) signaling. Cell viability was determined using a colorimetric assay with the MTS/PES solution. The mRNA levels were analyzed using reverse transcription quantitative polymerase chain reaction. The expression of NF-KB, AKT, and MAPK signaling proteins was measured using immunoblot analysis. Activin A did not affect THP-1 cell viability at concentrations below 50 ng/ml. Activin decreased the mRNA expression of cytokines (interleukin (IL)-1 beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha), toll-like receptor 4 (TLR4), and matrix metallo-proteinases (MMP)-9 proteins but did not affect IL-8 expression. Activin increased the expression of TLR2 and MMP-2. In addition, activin inhibited the phosphorylation of NF-KB p65, AKT, and MAPK (c-Jun N-terminal kinase (JNK), extracellular signal -regulated kinase (ERK), and p38 MAPK) signaling proteins. Our results suggest that activin may be involved in anti inflammation by inhibiting inflammatory gene expression and regulating NF-KB and AKT/MAPK signaling.Copyright: (c) 2023 by the C.M.B. Association. All rights reserved