During thioacetamide-induced acute liver failure, the proliferative response of hepatocytes to thyroid hormone is maintained, indicating a potential therapeutic approach to toxin-induced liver disease.

Abstract:

:In toxic liver injury, proliferation of preexisting hepatocytes helps restore liver mass and function. While loss of liver mass per se stimulates hepatocyte proliferation, exogenous mitogens have a potential role in enhancing liver regeneration. The aim of this study was to characterize the effects of the mitogen, tri-iodothyonine, on the regenerative capacity of hepatocytes during thioacetamide-induced liver failure. Rats received (two) thioacetamide injections and, 12 hr later, either tri-iodothyonine or vehicle-only control. Liver cell proliferation was assessed and comparison made with other control groups receiving tri-iodothyonine or vehicle only. In rats with thioacetamide-induced hepatitis the proportion of hepatocytes in S-phase was greater in the tri-iodothyonine group (27+/-3.5%) compared to the vehicle-only group (20+/-2.5%; P < 0.05), with, notably, a greater number of midzonal (BrdU) positive hepatocytes in the tri-iodothyonine group. We conclude that the ability of hepatocytes in the midzonal areas of rat liver to proliferate in response to tri-iodothyonine is maintained during severe acute toxic injury.

journal_name

Dig Dis Sci

authors

Malik R,Saich R,Rahman T,Hodgson H

doi

10.1007/s10620-006-9275-1

subject

Has Abstract

pub_date

2006-12-01 00:00:00

pages

2235-41

issue

12

eissn

0163-2116

issn

1573-2568

journal_volume

51

pub_type

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