Roxithromycin inhibits tumor necrosis factor‐α‐induced matrix metalloproteinase‐1 expression through regulating mitogen‐activated protein kinase phosphorylation and Ets‐1 expression

Abstract

Roxithromycin inhibits TNF-alpha-mediated MMP-1 induction through the downregulation of ERK1/2 and JNK activation and the subsequent reduction of Ets-1, suggesting that roxithromycin may have therapeutic use in periodontitis and other chronic inflammatory conditions involving MMP-1 induction.

Macrolides: from in vitro anti-inflammatory and immunomodulatory properties to clinical practice in respiratory diseases

“…In addition, it significantly inhibits TNFalpha-induced c-Jun N-terminal kinase activation (JNP) and marginally inhibits extracellular signal-regulated kinase (ERK)1/2 activation, but not p38 mitogen-activated protein kinase activation. The inhibition of TNF-mediated VEGF and induction of Ets-1 suggest the potential therapeutic utility of RXM in chronic inflammatory conditions [81,82].…”

TNF-α stimulates MMP-3 production via PGE2 signalling through the NF-kB and p38 MAPK pathway in a murine cementoblast cell line

“…17 Previous studies demonstrated the stimulating effect of TNF-a on MMP and TIMP expression by gingival fibroblasts, periodontal ligament fibroblasts and osteoblasts. [17][18][19][20][21][22][23] It is unknown, however, whether cementoblasts respond to this cytokine.…”

Immunomodulation and Anti-Inflammatory Effects of Macrolides: Old Drugs with Fascinating New Perspectives

“…RXM significantly inhibited TNFalpha-induced c-Jun N-terminal kinase activation (JNP) and marginally inhibited extracellular signal-regulated kinase (ERK) 1/2 activation, but not p38 mitogen-activated protein kinase activation. Furthermore, RXM reduced the induction of Ets-1, one of the critical factors in MMP-1 transcription [22]. The results of another study supported the antiinflammatory activities of AZM, since it was demonstrated that it reduced the levels of TNF-alpha and the inhibitions of NF-kappaB and specificity protein 1 (Sp1) DNA binding were proposed as possible mechanisms of this effect [23].…”