Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 1993;58(1):67-91.
doi: 10.1016/0163-7258(93)90067-n.

Liver cytoprotection by prostaglandins

J Quiroga  1 , J Prieto
Affiliations
Review

Liver cytoprotection by prostaglandins

J Quiroga et al. Pharmacol Ther. 1993.

Abstract

During the last decade intensive work on the relationships between the liver and the arachidonic acid cascade has greatly expanded our knowledge of this area of research. The liver has emerged as the major organ participating in the degradation and elimination of arachidonate products of systemic origin. The synthesis in the liver of arachidonate products derived from the cyclooxygenase, lipoxygenase and cytochrome P450 system pathways has been demonstrated. The participation of leukotriene B4 and cysteinyl-leukotrienes as mediators of liver damage and the possible therapeutic usefulness of prostaglandins (PGs) in acute liver injury has attracted the interest of clinicians. This article reviews the essential features regarding the role of arachidonate metabolites in liver disease and specially focuses on the cytoprotective effects on the liver displayed by PGE2, PGE1, PGI2 and synthetic PG analogs in experimental models of liver damage induced by ischemia-reperfusion injury, carbon tetrachloride, bacterial lipopolysaccharide and viral hepatitis and on the possible mechanisms underlying liver cytoprotection in these experimental models. The therapeutic usefulness of PGs in clinical practice is critically analyzed on the basis of available evidence in patients with fulminant hepatic failure and primary graft nonfunction following liver transplantation.

PubMed Disclaimer

References

    1. Abecassis M., Falk J.A., Makowka L., Dindzans V.J., Falk R.E., Levy G.A. 16,16 Dimethyl prostaglandin E2 prevents the development of fulminant hepatitis and blocks the induction of monocyte/macrophage procoagulant activity after murine hepatitis virus strain 3 infection. J. clin. Invest. 1987;80:881–889. - PMC - PubMed
    1. Aderem A., Cohen D., Wright S., Cohn Z. Bacterial lipopolysaccharides prime macrophages for enhanced release of arachidonic acid metabolites. J. exp. Med. 1986;164:165–179. - PMC - PubMed
    1. Alph M.H., Hickman R. The effect of prostaglandins, branched-chain amino acids and other drugs on the outcome of experimental acute porcine hepatic failure. J. Hepat. 1987;4:99–107. - PubMed
    1. Andreis P.G., Whitfield J.F., Armato U. Stimulation of DNA synthesis and mitosis of hepatocytes in primary cultures of neonatal rat liver by arachidonic acid and prostaglandins. Exp. Cell. Res. 1981;134:265–272. - PubMed
    1. Andreone P., Cursaro C., Ciriaci A.M., Buzzi A., Miniero R., Gasbarrini G. IFN-α increases PGE2 synthesis by cultured liver biopsies in patients with chronic active hepatitis. Gastroenterology. 1992;102:A775.