Abstract:
:The effects of cilostazol on stimulating heme oxygenase (HO)-1 expression including signal pathways and suppression of inflammatory cytokines and molecules were studied. Cilostazol stimulation time (1-8 h)- and concentration (1-30 μM)-dependently increased the HO-1 mRNA and protein expression associated with increased HO-1 activity, as did cobalt protoporphyrin IX (1-3 μM) in J774 macrophages. In addition, cilostazol (1-30 μM) concentration-dependently reduced lipopolysaccharide (LPS)-mediated nitrite and TNF-α production, in accordance with the inhibition of LPS-stimulated inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein expression in the J774 macrophages, as did CoPP (1 μM). In parallel with these results, LPS-induced IκBα degradation and NF-κB nuclear translocation were significantly decreased after treatment with cilostazol as well as with CoPP. These effects of cilostazol and CoPP were significantly reversed by Zn protoporphyrin IX (ZnPP). The effects of cilostazol on IκBα expression and nitrite production were not manifested in the cells transfected with HO-1 small interfering RNA. In the J774 macrophages, cilostazol time (0-180min)- and concentration (1-100μM)-dependently increased the nuclear expression of NF-E2 related factor (Nrf2) and antioxidant response element (ARE) activity (3.70±0.45 fold, P<0.01). PI3-kinase and Akt play a role in the major signal pathways with cilostazol-induced HO-1 expression. In summary, cilostazol suppressed production of anti-inflammatory cytokines and molecules via inhibition of NF-κB activation, through a mechanism involving up-regulation of cyclic AMP-dependent protein kinase activation-coupled Nrf2-linked HO-1 expression in J774A.1 macrophages.
journal_name
Immunol Lettjournal_title
Immunology lettersauthors
Park SY,Lee SW,Baek SH,Lee SJ,Lee WS,Rhim BY,Hong KW,Kim CDdoi
10.1016/j.imlet.2011.01.003subject
Has Abstractpub_date
2011-05-01 00:00:00pages
138-45issue
2eissn
0165-2478issn
1879-0542pii
S0165-2478(11)00024-1journal_volume
136pub_type
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