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Results for “LIVER REGENERATION”

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At least 19 recordsLinked to original sources

PubMed1997

Effects of octreotide on liver regeneration and tumour growth in the regenerating liver.

The ability of the liver to regenerate following resection is remarkable. However, there is evidence to suggest that tumour growth within the regenerating liver is significantly increased. As octreotide (a synthetic analogue of somatostatin) inhibits the growth and development of hepatic tumour in rats, we have investigated its effects on liver regeneration, liver blood flow, hepatic reticuloendothelial system activity and tumour growth in the rat following partial hepatectomy (PH). Octreotide significantly inhibited liver regeneration in the rat 1 and 2 weeks following PH when compared with controls (regeneration index: 1.0 and 1.14 cf. 1.14 and 1.4, respectively). There was no significant difference in hepatic arterial or portal venous blood flow following PH in control or octreotide-treated rats. However, portal pressure was significantly reduced in octreotide-treated rats. Hepatic reticuloendothelial system activity was significantly increased in octreotide-treated rats compared with control animals 1 and 2 weeks after hepatectomy (uptake of radiolabelled technetium-99m albumin colloid: 2.2 and 3.9 cf. 1.6 and 1.9). The growth of both HSN (fibrosarcoma) and K12-Tr (colonic adenocarcinoma) cells in the regenerating liver was significantly decreased by octreotide treatment compared with controls (median percentage hepatic replacement: HSN control 71.3%, Octreotide 8.4%, K12-Tr Control 38.3%, Octreotide 4.5%). The results of the present study demonstrate that octreotide inhibits both liver regeneration and tumour growth following PH, possibly via a similar mechanism.

Animals↗

PubMed1993

Interferon-gamma inhibits liver regeneration by stimulating major histocompatibility complex class II antigen expression by regenerating liver.

The effects of interferon-gamma and interleukin-2 on liver regeneration after 70% hepatectomy in rats was studied immunohistologically, with special attention paid to major histocompatibility complex class II antigen expression. Liver regeneration 2 days after partial hepatectomy as assessed on the basis of bromodeoxyuridine labeling index revealed that regeneration was inhibited significantly in rats given a single dose of interleukin-2 or interferon-gamma compared with rats that underwent only partial hepatectomy. Simultaneous administration of interleukin-2 and interferon-gamma inhibited liver regeneration more markedly than administration of either drug. In rats subjected to partial hepatectomy, Kupffer cells around the portal vein expressed slightly more major histocompatibility complex class II antigen than did sham-operated controls. In the group given interferon-gamma, major histocompatibility complex class II antigen expression was markedly increased. Major histocompatibility complex class II antigen expression was greatest in most Kupffer cells of rats given both interleukin-2 and interferon-gamma. These results suggest that interferon-gamma activates (proliferating) Kupffer cells, in turn leading to suppression of liver regeneration. These major histocompatibility complex class II antigen-positive Kupffer cells act as antigen-presenting cells and present hepatocyte as antigen, the so-called abnormal self, to helper and cytotoxic T cells. Both types of T cells, in turn, may suppress hepatocyte proliferation. The various cytokines induced by the activated Kupffer cells and helper T cells seem to form a network with interferon-gamma to regulate liver regeneration.

Animals↗

PubMed1997

[Increase in the level of augmenter of liver regeneration mRNA in the rat regenerating liver after partial hepatectomy].

Augmenter of liver regeneration (ALR) is a novel hepatic stimulator. After 70% of the rat liver was removed, ALR-like activity in the remnant liver began to increase within 24 h. In parallel with the activity, the ALR mRNA level in the remnant liver increased 12 h after the operation and reached a maximum in 24 h. These findings indicate that the liver itself produces ALR, which may be a hepatotropic factor acting as a trigger for liver regeneration.

Animals↗

PubMed1978

Superoxide dismutase activity of normal murine liver, regenerating liver, and H6 hepatoma.

By means of both direct assay and gel electrophoresis, normal A/J mouse liver was shown to possess both Cu-Zn and Mn superoxide dismutase (SD) activity. H6 hepatoma cells contained Cu-Zn SD activity, but no Mn SD activity was detectable. Isolated mitochondria from normal liver contained both forms of the enzyme, but isolated mitochondria from H6 hepatoma cells contained no SD activity. To ascertain whether this loss of Mn SD activity was characteristic of these tumor cells or was simply a property of rapidly dividing cells, SD activity was measured in regenerating liver. Mn SD activity was present in the regenerating liver at all times after surgery. Hence loss of the Mn SD activity seemed to be a characteristic of some tumor cells but not of corresponding rapidly dividing normal cells.

Animals↗

PubMed1981

DNA methylase activity of normal liver, regenerating liver, and a transplantable hepatocellular carcinoma.

DNA from transplantable hepatocellular carcinoma (THC) 252 has recently been found to have a lower 5-methylcytosine content than DNA from normal or regenerating rat liver. We have determined that DNA methylase, purified 200-fold from nuclei of regenerating rat liver, can add more methyl groups to THC 252 DNA than to DNA from normal or regenerating rat liver. Furthermore, a similarly purified DNA methylase from THC 252 was found to methylate THC 252 DNA at a higher rate than it methylated DNA from normal or regenerating liver. The larger number of unmethylated sites in THC 252 DNA was not due to a deficiency of DNA methylase since the level of methylase activity of nuclear extracts from THC 252 was 2.7 times that of normal liver and 1.5 times that of regenerating liver. Methylases from these three sources had similar rats of reaction with different DNA substrates. These findings suggest that the hypomethylation of THC 252 DNA is not due to decreased methylase activity or to altered enzyme specificity.

Animals↗

PubMed1998

Liver regeneration, liver cancers and cyclins.

Accumulating evidence has revealed that malignant cell growth is regulated by complex mechanisms involved in genetic and epigenetic factors. Among human cancers, cancer in the liver (hepatocellular carcinoma (HCC)) is characterized by the evidence that it is usually based on chronic liver diseases such as liver cirrhosis or chronic hepatitis, in which the liver is persistently regenerating following hepatic injury. This raises the possibility that repeated hepatocyte proliferation may cause disorder of genes that are regulating the cell cycle in hepatocytes, thus causing HCC. In this article, recent studies focusing on liver regeneration and cancer are reviewed from the viewpoint of the cell cycle that is regulated by cyclin and the associated proteins.

Carcinoma, Hepatocellular↗

PubMed1964