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 |
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Authors: | Raza Malik Rebecca Saich Tony Rahman Humphrey Hodgson |
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Institution: | (1) Centre for Hepatology, Department of Medicine, Royal Free Campus, Royal Free and University College Medical School, Rowland Hill Street, Hampstead, London, United Kingdom, NW3 2PF |
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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. |
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Keywords: | Primary mitogen Acute hepatic failure Thyroid hormone T3 Thioacetamide |
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