Platonin, a photosensitizing
dye, is known to possess
antioxidant and anti-inflammatory activity.
Platonin has been used to treat
trauma,
ulcers and some acute
inflammations and it also reported to improve blood circulation and reduce mortality in
endotoxin-induced rat models. Our previous studies established that
platonin suppresses the
lipopolysaccharides (LPS)-induced inflammatory
cytokines, including interleukin-1β (IL-1β-+),
IL-6,
tumor necrosis factor-α (TNF-α), and
inducible nitric oxide synthase (iNOS). Nuclear factor-kB (
NF-kB) and
activator protein-1 (AP-1)
transcription factors are reported to be essential in mediating the
endotoxin-induced production of inflammatory molecules. In vivo studies from our groups revealed that
platonin has potential effects on inhibiting
pyrogen release, tissue damage and
ischemia during
heatstroke,
ischemia reperfusion injury in lungs and also improve the survival of skin allografts in rats. Clinically, this compound has been proven to cure
juvenile rheumatoid arthritis (JRA) and
polyarteritis nodosa (PN). In this review, we summarize the pharmacological and clinical effects of
platonin via describing the potential molecular mechanism of regulation of inflammatory molecules of
mitogen-activated protein kinases (MAPKs), including extracellular regulated
kinase (ERK),
c-jun N-terminal kinase (JNK), and
p38 MAPK and also
NF-kB activation. Moreover, this paper discusses the signaling pathways expedited by
NF-kB,
AP-1, MAPKs and NO/NOS, these all have been reflected in inflammatory processes, and could be the encouraging molecular targets for the design of
pharmaceutical drugs targeting antiinflammatory
therapy.