AIM To examine the expression of activin A, amember of the transforming growth factor (TGF-β) superfamily, recently has been reported to beoverexpressed in liver cirrhosis, in the course ofcarbon tetrachloride-induced rat hepaticfibrosis.METHODS Hepatic fibrosis was induced in ratsby subcutaneous injections of 40% carbontetrachloride oily solution for a period of I to 7weeks. At the end of 1, 2, 3, 4, 5, 6 and 7 weeksafter carbon tetrachloride injections, the ratswere killed in group (6-10 rats each time) forstudy. The activin A messenger RNA expressionand its protein localization were assessed bysemi-quantitative reverse transcriptionpolymerase chain reaction (RT-PCR) andimmunohistochemistry.RESULTS The normal rat liver expressedactivin A mRNA and protein, and its expressionwas transiently decreased and becameundetectable after carbon tetrachlorideinjections for 2 or 3 weeks and then increasedgradually. After injection of carbon tetrachloridefor 6 and 7 weeks, activin A mRNA and proteinexpressions were significantly enchanced in ratliver. Compared with that of the normal ratliver. Activin A mRNA expression levels in ratsreceiving carbon tetrachloride injections for 6and 7 weeks were 1.6 and 2.2 times that of thosein normal rat liver respectively (0.456±0.094 vs0.286±0.0670, P<0.01; 0. 620±0.134 vs 0.286 ±0.0670, P<0.01 ). Immunohistochemistryshowed that activin A expressed in hepatocytesof normal liver, and its expression wasdecreased in rats receiving carbon tetrachloridefor 2 or 3 weeks. Compared with normal liver,activin A expression distribution mode changedin fibrotic liver, being increased significantly inhepatocytes around fibrotic areas.CONCLUSION Activin A expression wasincreased in late stage of hepatic fibrosis, andthis may be involved in hepatic fibrosisformation in this period. AIM To examine the expression of activin A, a member of the transforming growth factor (TGF-β) superfamily, recently has been reported to beoverexpressed in liver cirrhosis, in the course ofcarbon tetrachloride-induced rat hepatic fibrosis. METHODS Hepatic fibrosis was induced in ratsby subcutaneous At the end of 1, 2, 3, 4, 5, 6 and 7 weeks after carbon tetrachloride injections, the rats were killed in group (6-10 rats each time) injections of 40% carbon tetrachloride oily solution for a period of 1 to 7 weeks. forstudy. The activin A messenger RNA expression and its protein localization were assessed by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry. RESULTS The normal rat liver expressed activin A mRNA and protein, and its expression was transiently decreased and became undetectable after carbon tetrachloride injection for 2 or 3 weeks and then increasedgradually. After injection of carbon tetrachloride for 6 and 7 weeks, activin A mRNA and prot Compared with that of the normal rat liver. Activin A mRNA expression levels in ratsreceiving carbon tetrachloride injections for 6 and 7 weeks were 1.6 and 2.2 times that of thosein normal rat liver respectively (0.456 ± 0.094 vs 0.286 ± 0.0670 , P <0.01; 0. 620 ± 0.134 vs 0.286 ± 0.0670, P <0.01). Immunohistochemistryshowed that activin A expressed in hepatocytes of normal liver, and its expression wascreased in rats receiving carbon tetrachloride for 2 or 3 weeks. Compared with normal liver, activin A expression distribution mode changed in fibrotic liver, being much significantly in hepatocytes fibrotic areas. CONCLUSION Activin A expression was reinforced in late stage of hepatic fibrosis, and may be involved in hepatic fibrosis formation in this period.