Prostaglandin synthesis and early biochemical events in the liver cells during the acute-phase response.
Acetylsalicic acid and indomethacin suppress the increase of alpha-amanitin sensitive RNA synthesis (pre-mRNA), but not that of alpha-amanitin resistant RNA synthesis (pre-rRNA), which occur in liver nuclei a few hours after the start of turpentine-induced inflammation in the skin. The inflammation-associated increase in activity of nuclear ATP-ase is also prevented. Synthesis of prostaglandins PGE2 and PGE2 alpha by liver microsomes from turpentine-treated rats is enhanced within 90 min. from treatment. The results suggest an important role of intracellular prostaglandins as mediators of the early nuclear events occurring in the liver at the beginning of the acute-phase response to inflammation.
D000210:Acute-Phase Reaction / Q000139:chemically induced / Q000378:metabolism*; D000818:Animals; D001241:Aspirin / Q000494:pharmacology; D015237:Dinoprost; D015232:Dinoprostone; D007213:Indomethacin / Q000494:pharmacology; D007249:Inflammation / Q000378:metabolism*; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D009694:Nucleic Acid Precursors / Q000096:biosynthesis; D011458:Prostaglandins E / Q000096:biosynthesis*; D011460:Prostaglandins F / Q000096:biosynthesis*; D012322:RNA Precursors; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D011919:Rats, Inbred Strains; D014425:Turpentine
D009694:Nucleic Acid Precursors; D011458:Prostaglandins E; D011460:Prostaglandins F; D012322:RNA Precursors; D012333:RNA, Messenger; D015237:Dinoprost; D015232:Dinoprostone; D001241:Aspirin; D014425:Turpentine; D007213:Indomethacin