Decreased prostacyclin production by liver non-parenchymal cells precedes liver injury in experimental alcoholic liver disease.
We used the intragastric feeding rat model for alcoholic liver disease to investigate the relationship between prostacyclin and liver injury. Rats were fed the following diets for periods ranging from 1 to 8 weeks: corn oil plus ethanol (CO+E), corn oil plus dextrose (CO+D), saturated fat plus ethanol (SF+E) and saturated fat plus dextrose (SF+D). Prostacyclin production (assessed by 6-ketoprostaglandin F1 alpha) by liver non-parenchymal cells decreased steadily over the 8 week period in animals fed CO+E (liver injury present) whereas in animals fed SF+E (no liver injury) there was no change in prostacyclin production. Plasma levels of 6-ketoprostaglandin F1 alpha were also significantly lower in the CO+E group compared to the other groups studied. We propose that decreased prostacyclin production by liver non-parenchymal cells may contribute to the hepatotoxic effect of ethanol.
Nanji
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AA
Department of Pathology, New England Deaconess Hospital, Boston, MA.
Khwaja
S
S
Sadrzadeh
S M
SM
D015121:6-Ketoprostaglandin F1 alpha / Q000032:analysis; D000818:Animals; D004195:Disease Models, Animal; D011464:Epoprostenol / Q000096:biosynthesis*; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D008108:Liver Diseases, Alcoholic / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar
D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol