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.
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