Doxycycline inhibits bacterial protein synthesis by binding to the 30S ribosomal subunit. Doxycycline has bacteriostatic activity against a broad range of Gram-positive and Gram-negative bacteria.
Among the tetracycline group of compounds, doxycycline blocked and reversed both spontaneous and interleukin 1β-induced OA-NOS activity in ex vivo conditions. Similarly, doxycycline inhibited lipopolysaccharide- and interferon-γ-stimulated iNOS in RAW 264.7 cells in vitro, as assessed by nitrite accumulation. Although both these enzyme isoforms could be inhibited by doxycycline , their susceptibility to this drugs was distinct.