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. 2007 Oct 29;153(Suppl 1):S200–S215. doi: 10.1038/sj.bjp.0707489

Table 2. Impact of anti-inflammatory agents on LX, RV and PD: biosynthesis, inactivation and receptors.

Anti-inflammatory agent Impact
NSAID
 Aspirin Switches COX-2 activity to produce 15R-HETE (from AA; Clària and Serhan, 1995), 18R-HEPE (from EPA; Serhan et al., 2000), and 17R-HDHA (from DHA; Serhan et al., 2002)
  Increases ATL formation in vivo in experimental animals (reviewed in Chiang et al., 2006) and in human (Chiang et al., 2004)
  Initiates RvE1 formation in vivo in experimental animals (Serhan et al., 2000) and in human (Arita et al., 2005a)
  Initiates RvD formation in vivo in experimental animals (Serhan et al., 2002)
  Inhibits 15-PGDH (Hansen, 1974)
 Indomethacin Permits 18R-HEPE generation with recombinant COX-2, yet reduces its levels (Serhan et al., 2000)
  Inhibits 15-PGDH (Cho and Tai, 2002; Hansen, 1974) and EOR (Clish et al., 2001)
 Acetaminophen Permits 18R-HEPE generation with recombinant COX-2, yet reduces its levels (Serhan et al., 2000)
 Diclofenac Inhibits EOR (Clish et al., 2001)
   
Steroid
 Dexamethasone Upregulates 5-LOX expression (Colamorea et al., 1999; Uz et al., 2001)
  Inhibits 15-PGDH (cell-type dependent) (Tong and Tai, 2000)
  Upregulates ALX receptor (Hashimoto et al., 2007; Sawmynaden and Perretti, 2006)
   
Thiazolidinedione
 Pioglitazone Increases LXA4 and 15-epi-LXA4 formation (Birnbaum et al., 2006)
 Ciglitazone Inhibits 15-PGDH (Cho and Tai, 2002)
   
Statin
 Atorvastatin Increase LXA4 and 15-epi-LXA4 formation (Birnbaum et al., 2006)

Abbreviations: 15-PGDH; 15-hydroxyprostaglandin dehydrogenase; 18R-HEPE, 18R-hydroxyeicosapentaenoic acid; AA, arachidonic acid; ATL, aspirin-triggered LX; COX-2, cyclooxygenase-2; EOR, eicosanoid oxidoreductase; DHA, docosahexaenoic acid; 5-LOX, 5-lipoxygenase; LXA4, lipoxin A4; NSAID, nonsteroidal anti-inflammatory drug; Rv, resolvin.