Histone deacetylase inhibitors (HDACi) are currently used in the routine clinical treatment of
cancer. Alongside the antitumor activity of HDACi, increased attention has been paid to their anti‑inflammatory effects. The present study aimed to analyze the inhibitory effects of the HDACi
Trichostatin A (
TSA), on the release of inflammatory mediators from macrophages differentiated from U‑937 cells. A low dose of
TSA (50 nM) was able to effectively decrease the levels of inflammatory
cytokines in the cell supernatants, independent of apoptosis. In addition, the potential underlying mechanisms were explored, and
TSA was shown to promote, rather than inhibit, the acetylation of
histones. Furthermore, the inflammation‑induced enhanced expression of class I HDACs was effectively inhibited by
TSA. In addition,
TSA enhanced the
lipopolysaccharide (LPS)‑induced expression of cyclooxygenase‑2, but suppressed the LPS‑induced expression of
chemokine (C‑C motif)
ligand 7. The acetylation level of nuclear factor‑κB p65 was decreased by LPS, but increased following treatment with
TSA. In conclusion,
TSA was able to inhibit
inflammation in macrophages. However, whether the mechanism by which
TSA inhibits
inflammation is through significantly enhancing
histone acetylation, in order to selectively suppress the expression of proinflammatory genes, and/or through regulating non‑histone acetylation requires further research.