Hepatic stimulator substance （HSS） has been referred to as a liver-specific but species non-specific growth factor. Gradient purification and sequence analysis of HSS protein indicated that it contained the augmente...Hepatic stimulator substance （HSS） has been referred to as a liver-specific but species non-specific growth factor. Gradient purification and sequence analysis of HSS protein indicated that it contained the augmenter of liver regeneration （ALR）, also known as hepatopoietin （HPO）. ALR, acting as a hepatotrophic growth factor, specifically stimulated proliferation of cultured hepatocytes as well as hepatoma cells in vitro, promoted liver regeneration and recovery of damaged hepatocytes and rescued acute hepatic failure in vivo. ALR belongs to the new Erv1/Alr protein family, members of which are found in lower and higher eukaryotes from yeast to man and even in some double-stranded DNA viruses. The present review article focuses on the molecular biology of ALR, examining the ALR gene and its expression from yeast to man and the biological function of ALR protein. ALR protein seems to be non-liver-specific as was previously believed, increasing the necessity to extend research on mammalian ALR protein in different tissues, organs and developmental stages in conditions of normal and abnormal cellular growth.展开更多
Objective To clarify the actions of somatostatin （SST） on the hepatic fibrogenesis in experimental rats. Methods Seventy five Sprague-Dawley rats were divided into 5 groups at random, including normal control, model...Objective To clarify the actions of somatostatin （SST） on the hepatic fibrogenesis in experimental rats. Methods Seventy five Sprague-Dawley rats were divided into 5 groups at random, including normal control, model control, SST-treated model groups of high, medium and low doses （200 μg·kg^-1·d^-1 , 100μg·kg^ 1 ·d^-1and 50 μg·kg^ 1 ·d^-1, respectively） （ n = 15, in each group）. All rats, except for the normal controls, were injected with 40% carbon tetrachloride （ CCI4 ） subcutaneously for 8 weeks to establish hepatic fibrosis. Meanwhile, rats of SST-treated model groups were given different doses of SST twice a day in the same way. Then the liver function, serum levels of hyaluronic acid （HA）, laminin （ LM） , and collagen type IV （CIV） were tested. The collagen types I and III, and pathological changes in liver tissue were assessed. Results Being compared with the model control group, SST-treated groups, especially the medium and low dose ones, exhibited significantly improved indices of liver function, including alanine minotransferase （ALT）, aspartate aminotrans- ferase （AST）, albumin （ALB）, total bilirubin （TBIL） and alkaline phosphatase （ALP）. Markedly lowered expres- sion of serum HA, LM and tissular collagen types I, III were also detected radioimmunologically and immunohisto- chemically in the low dose SST-treated model group. Moreover, pathological findings, such as lessened fibrous septa, decreased hepatic stellate cells （HSCs）, alleviated hepatic steatosis and attenuated inflammation, confirmed the significant improvement in fibrotic degree under the treatment of low dose rather than other doses of SST. Conclusion SST exerts the negative modulatory effect on hepatic fibrosis with a pathophysiological basis of extra- cellular matrixes （ECM） decreasing and hepatocyte protection. Low dose of SST （50 μg·kg^ 1 ·d^-1 ） maY be the optimum one among all doses.展开更多
文摘Hepatic stimulator substance （HSS） has been referred to as a liver-specific but species non-specific growth factor. Gradient purification and sequence analysis of HSS protein indicated that it contained the augmenter of liver regeneration （ALR）, also known as hepatopoietin （HPO）. ALR, acting as a hepatotrophic growth factor, specifically stimulated proliferation of cultured hepatocytes as well as hepatoma cells in vitro, promoted liver regeneration and recovery of damaged hepatocytes and rescued acute hepatic failure in vivo. ALR belongs to the new Erv1/Alr protein family, members of which are found in lower and higher eukaryotes from yeast to man and even in some double-stranded DNA viruses. The present review article focuses on the molecular biology of ALR, examining the ALR gene and its expression from yeast to man and the biological function of ALR protein. ALR protein seems to be non-liver-specific as was previously believed, increasing the necessity to extend research on mammalian ALR protein in different tissues, organs and developmental stages in conditions of normal and abnormal cellular growth.
基金Supported by Scientific Development Programs of Science and Technology Commission of Shanghai(004119047)
文摘Objective To clarify the actions of somatostatin （SST） on the hepatic fibrogenesis in experimental rats. Methods Seventy five Sprague-Dawley rats were divided into 5 groups at random, including normal control, model control, SST-treated model groups of high, medium and low doses （200 μg·kg^-1·d^-1 , 100μg·kg^ 1 ·d^-1and 50 μg·kg^ 1 ·d^-1, respectively） （ n = 15, in each group）. All rats, except for the normal controls, were injected with 40% carbon tetrachloride （ CCI4 ） subcutaneously for 8 weeks to establish hepatic fibrosis. Meanwhile, rats of SST-treated model groups were given different doses of SST twice a day in the same way. Then the liver function, serum levels of hyaluronic acid （HA）, laminin （ LM） , and collagen type IV （CIV） were tested. The collagen types I and III, and pathological changes in liver tissue were assessed. Results Being compared with the model control group, SST-treated groups, especially the medium and low dose ones, exhibited significantly improved indices of liver function, including alanine minotransferase （ALT）, aspartate aminotrans- ferase （AST）, albumin （ALB）, total bilirubin （TBIL） and alkaline phosphatase （ALP）. Markedly lowered expres- sion of serum HA, LM and tissular collagen types I, III were also detected radioimmunologically and immunohisto- chemically in the low dose SST-treated model group. Moreover, pathological findings, such as lessened fibrous septa, decreased hepatic stellate cells （HSCs）, alleviated hepatic steatosis and attenuated inflammation, confirmed the significant improvement in fibrotic degree under the treatment of low dose rather than other doses of SST. Conclusion SST exerts the negative modulatory effect on hepatic fibrosis with a pathophysiological basis of extra- cellular matrixes （ECM） decreasing and hepatocyte protection. Low dose of SST （50 μg·kg^ 1 ·d^-1 ） maY be the optimum one among all doses.
