Peroxisome proliferator-activated receptor gamma (PPAR γ), is important in the immunoregulation of the allergic response. Mast cells are the most important inflammatory cells in immediate hypersensitivity and allergic diseases. However, there is limited information regarding the effects of PPAR γ on mast cell maturation. In the present study, mouse bone marrow‑derived mast cells (BMMCs) were cultured in interleukin (IL)‑3 and stem cell factor (SCF), in the presence or absence of the PPAR γ agonist, pioglitazone (PIO). The expression levels of the tyrosine kinase receptor CD117 and the high affinity IgE receptor FcεRI α, were assessed by flow cytometry, cell viability was assessed by Alamar‑Blue assay and histamine release was determined by measuring the activity of β‑hexosaminidase. IL‑3 and SCF are required for the development of mast cells in vitro. PIO dose‑dependently inhibited the expression of CD117 and FcεRI α, and the maturation of BMMCs. Treatment with PIO additionally inhibited the formation of granules and reduced the expression of β‑hexosaminidase. In addition, reverse transcription‑polymerase chain reaction analysis revealed that BMMCs treated with PIO expressed a lower level of mast cell protease (MCP)‑6 mRNA and PIO treatment enhanced the level of PPAR γ mRNA. Furthermore, PIO induced mast cell progenitor apoptosis. PPAR γ agonists may maintain mast cell homeostasis by inhibiting maturation of their precursors. The inhibitory effects of PPAR γ agonists include suppression of the activation of mast cells and a decrease in mast cell function in the inflammatory response. Therefore, PPAR γ agonists may serve as effective anti-inflammatory reagents in the treatment of allergic reactions.