AIM:To investigate the effects and molecular mechanismsof recombinant human growth hormone(rhGH)onprotecting liver function and alleviating portal hypertensionof liver cirrhotic rats.METHODS:Liver cirrhosis of male Sprague-Dawley ratswas induced by administration of thioacetamide.The ratswith or without liver cirrhosis were randomly divided intofour groups.Group A consisted of the normal rats wastreated with normal saline(NS),group B consisted of thenormal rats was treated with rhGH,group C consisted ofcirrhotic rats was treated with NS,and group D consistedof cirrhotic rats was treated with rhGH.The rats of differentgroups were subcutaneously injected with 0.5 mL of NS or333 ng/kg of rhGH daily for 7 d.After treatments,thefollowing parameters were examined,including GH-bindingcapacity(R_T)by ~(125)I-hGH binding,growth hormone receptormRNA(GHR mRNA)expression by RT-PCR,relative contentof collagen(RCC)by histomorphomertry,and level ofmalon-dialdehyde(MDA)and superoxide dismutase(SOD)in liver tissue by thiobarbituric acid reaction and pyrogallicacid self-oxidation,respectively.Serum albumin(ALB),alanine transaminase(ALT)and portal vein pressure(PVP)were also examined.RESULTS:rhGH up-regulated both the GH-binding capacity(R_T)and the expression of GHR mRNA in vivo.RT in groupA(72±12 fmol/mg protein)was significantly higher thanthat in group C(31±4 fmol/mg protein)(P<0.05).R_T ingroup B (80±9 fmol/mg protein)increased markedlycompared to group A(P<0.05).R_T in group D(40±7 fmol/mgprotein)raised remarkably compared with group C(P<0.05),but less than that in group A,and there was no significantGH binding affinity contrast(Kd)change.The GHR mRNAlevel(iOD,pixel)in group A(29±3)was significantly higherthan that in group C(23±3)(P<0.05).GHR mRNA levelswere significantly raised in group B(56±4)and group D(42±8)compared with groups A and C(29±3 and 23±3,respectively)(P<0.05).Compared with the normal liver, MDA level was higher and SOD level was lower in cirrhoticlivers.After rhGH treatment,MDA level was significantlydeclined to 12.0±2.2 nmol/mg protein and SOD was raisedto 1029±76 U/mg protein in group D(P<0.05).ALB levelsin groups B and D(42±7 g/L and 37±7 g/L,respectively)were significantly raised compared with those in groups Aand C(35±5 g/L and 29±4 g/L,respectively)(P<0.05).ALT level was markedly lower in group D(69±7 U/L)compared to group C(89±15 U/L)(P<0.05),and close togroup A(61±10 U/L).RCC in group C(22.30±3.86%)wassignificantly higher than that in group A(1.14±0.21%)andgroup D(14.70±2.07%)(P<0.05).In addition,rhGHmarkedly alleviated portal hypertension in liver cirrhoticrats(group D vs C,9.3±1.5 cmH_2O vs 14.4±2.0 cmH_2O)(P<0.05).CONCLUSION:Pharmacological doses of rhGH canincrease R_T and GHR mRNA expression,ameliorate liverfunctions,repress fibrosis and decline portal hypertension,suggesting it has potentially clinical usage as a hepatotropicfactor. To investigate the effects and molecular mechanisms of recombinant human growth hormone (rhGH) onprotecting liver function and alleviating portal hypertensionof liver cirrhotic rats. METHODS: Liver cirrhosis of male Sprague-Dawley ratswas induced by administration of thioacetamide.The rats with or without liver cirrhosis were randomly divided intofour groups. Group A consisted of normal rats wastreated with normal saline (NS), group B consisted of normal rats was treated with rhGH, group C consisted of chronic rats was treated with NS, and group D consisted of cirrhotic rats was treated with rhGH.The rats of different groups were were subcutaneously injected with 0.5 mL of NS or 333 ng / kg of rhGH daily for 7 d. After treatments, the following parameters were examined, including GH-binding capacity (R_T) by ~ (125) growth hormone receptormRNA (GHR mRNA) expression by RT-PCR, relative content of collagen (RCC) by histomorphomertry, and level of malon-dialdehyde (MDA) and superoxide dismutase liver tissue by thiobarbituric acid reaction and pyrogallic acid self-oxidation, respectively.Serum albumin (ALB), alanine transaminase (ALT) and portal vein pressure (PVP) were also examined .RESULTS: rhGH up-regulated both the GH- binding capacity ) and the expression of GHR mRNA in vivo. RT in group A (72 ± 12 fmol / mg protein) was significantly higher thanthat in group C (31 ± 4 fmol / mg protein) 9 fmol / mg protein increased markedlycompared to group A (P <0.05) .R_T in group D (40 ± 7 fmol / mgprotein) raised remarkably compared with group C (P <0.05), but less than that in group A, and there was no significant GH binding affinity (Kd) change.The GHR mRNAlevel (iOD, pixel) in group A (29 ± 3) was significantly higherthan that in group C (23 ± 3) raised in group B (56 ± 4) and group D (42 ± 8) compared with groups A and C (29 ± 3 and 23 ± 3, respectively) (P <0.05) .Compared with the normal liver, MDA level was higher and SOD level was lower in cirrhoticliver s.After rhGH treatment, MDA level was significantly decreased to 12.0 ± 2.2 nmol / mg protein and SOD was raised to 1029 ± 76 U / mg protein in group D (P <0.05). ALB levels in groups B and D (42 ± 7 g / L and 37 ± 7 g / L, respectively) were significantly raised compared to those in groups Aand C (35 ± 5 g / L and 29 ± 4 g / L, respectively) (P <0.05) 69 ± 7 U / L) compared to group C (89 ± 15 U / L) (P <0.05) and close togroup A (61 ± 10 U / L) .RCC in group C (22.30 ± 3.86%) wassignificantly higher than that in group A (1.14 ± 0.21%) and group D (14.70 ± 2.07%) (P <0.05) .In addition, rhGHmarkedly elevated portal hypertension in liver cirrhoticrats (group D vs C, 9.3 ± 1.5 cmH 2 O vs 14.4 ± 2.0 cmH 2 O ) (P <0.05). CONCLUSION: Pharmacological doses of rhGH canincrease R_T and GHR mRNA expression, ameliorate liverfunctions, repress fibrosis and decline portal hypertension, suggesting it has affected clinical usage as a hepatotropicfactor.