Chronic inflammation in adjuvant arthritic rats correlates with enhancement of 12-L-HETE-synthesis.
The development of chronic inflammation in adjuvant arthritic rats was found to be strongly correlated with the appearance in serum of a factor (HSF) which enhanced the formation of 12-L-HETE by platelet-lipoxygenase, and with the serum-concentration of 12-L-HETE. The latter was determined by scanning at 235 nm after extraction and high performance thin-layer chromatography. Arthritic rat platelet-rich plasma (PRP) converted exogenous arachidonic acid to 12-L-HETE at a rate 2.6-fold higher than control rat PRP. By resuspending arthritic rat platelets in normal rat plasma, and normal rat platelets in arthritic rat plasma, this increase in conversion rate was found to be caused by HSF present in the arthritic rat plasma. Treatment of arthritis with non-steroidal anti-inflammatory drugs inhibited HSF activity as well as the increase in serum-12-L-HETE concentration, which indicates a prostaglandin-mediated mechanism of HSF synthesis or release.
D019377:12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001095:Arachidonic Acids / Q000096:biosynthesis*; D001168:Arthritis / Q000378:metabolism*; D001169:Arthritis, Experimental / Q000378:metabolism*; D002908:Chronic Disease; D005260:Female; D007249:Inflammation / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains
D000893:Anti-Inflammatory Agents; D001095:Arachidonic Acids; D019377:12-Hydroxy-5,8,10,14-eicosatetraenoic Acid