AIM:To investigate the expression of growth hormonereceptor(GHR)and mRNA of GHR in cirrhotic livers of ratswith the intension to find the basis for application ofrecombinant human growth hormone(rhGH)to patients withliver cirrhosis.METHODS:Hepatic cirrhosis was induced in Sprague-Dawley rats by administration of thioacetamideintraperitoneally for 9-12 weeks.Collagenase Ⅳ wasperfused in situ for isolation of hepatocytes.The expressionof GHR and its mRNA in cirrhotic livers was studied withradio-ligand binding assay,RT-PCR and digital imageanalysis.RESULTS:One class of specific growth hormone-bindingsite,GHR,was detected in hepatocytes and hepatic tissueof cirrhotic livers.The binding capacity of GHR(R_T,fmol/mgprotein)in rat cirrhotic liver tissue(30.8±1.9)was significantlylower than that in normal control(74.9±3.9)at the timepoint of the ninth week after initiation of induction of cirrhosis(n=10,P<0.05),and it decreased gradually along with theaccumulation of collagen in the process of formation anddevelopment of liver cirrhosis(P<0.05).The number ofbinding sites(×10~4/cell)of GHR on rat cirrhotic hepatooltes(0.86±0.16)was significantly lower than that(1.28±0.24)in conytrol(n=10,P<0.05).The binding affinity of GHR amongliver tissue,hepatocytes of various groups had no significantdiligence(P>0.05).The expression of GHR mRNA(riOD,pixel)in rat cirrhotic hepatic tissues(23.3±3.1)was alsosignificantly lower than that(29.3±3.4)in normal control(n=10,P<0.05). CONCLUSION:The growth hormone receptor wasexpressed in a reduced level in liver tissue of cirrhotic rats,and lesser expression of growth hormone receptors wasfound in a later stage of cirrhosis.The reduced expressionof growth hormone receptor was partly due to its decreasedexpression on cirrhotic hepatocytes and the reducedexpression of its mRNA in cirrhotic liver tissue. AIM: To investigate the expression of growth hormone receptor (GHR) and mRNA of GHR in cirrhotic livers of rats with the intension to find the basis for application of recombinant human growth hormone (rhGH) to patients with liver cirrhosis. METHODS: Hepatic cirrhosis was induced in Sprague- Dawley rats by administration of thioacetamide intravenously for 9-12 weeks. Collagenase IV was perfused in situ for isolation of hepatocytes. The expression of GHR and its mRNA in cirrhotic livers was studied with radio-ligand binding assay, RT-PCR and digital image analysis .RESULTS: One class of specific growth hormone-binding sites, GHR, was detected in hepatocytes and hepatic tissue of cirrhotic livers.The binding capacity of GHR (R_T, fmol / mg protein) in rat cirrhotic liver tissue (30.8 ± 1.9) was significantlylower than that in normal control ± 3.9) at the timepoint of the ninth week after initiation of induction of cirrhosis (n = 10, P <0.05), and it ultimately followed along with the acumulation of collagen in the proces s of formation and development of liver cirrhosis (P <0.05). The number of binding sites (× 10 ~ 4 / cell) of GHR on rat cirrhotic hepatomates (0.86 ± 0.16) was significantly lower than that (1.28 ± 0.24) in conytrol = 10, P <0.05). The binding affinity of GHR amongliver tissue, hepatocytes of various groups had no significant diligence (P> 0.05). The expression of GHR mRNA (riOD, pixel) in rat cirrhotic hepatic tissues (23.3 ± 3.1) was CONCLUSION: The growth hormone receptor wasexpressed in a reduced level in liver tissue of cirrhotic rats, and lesser expression of growth hormone receptors was found in a (26.3 ± 3.4) in normal control (n = 10, later stage of cirrhosis. The reduced expression of growth hormone receptor was partly due to its decrease index on cirrhotic hepatocytes and the reducedexpression of its mRNA in cirrhotic liver tissue.