During the last several decades, our knowledge of the cellular and molecular mechanisms of liver fibrosis has greatly advanced. The events of hepatic fibrogenesis have become better understood and it has been recognized that even advanced liver fibrosis is reversible; researchers have been stimulated to identify antifibrotic therapies. The hepatic stellate cell (Ito cell, fat-storing cell, lipocyte, perisinusoidal cell) is central to fibrogenesis; its proliferation may be stimulated by a number of factors, thus enhancing fibrogenesis.To elucidate the role of Kupffer cells in liver fibrosis and cirrhosis, rats were treated with GdCl₃ and biliary cirrhosis was induced by ligation of the common bile duct. The level of hepatic collagen increased significantly in the bile duct-ligated rats, whereas GdCl₃ prevented the increase in collagen content, as evidenced by the liver hydroxyproline content and by the results of histopathological analysis. It is reasonable to postulate that the inhibition of Kupffer cells with GdCl₃ could disrupt the sequence of events leading to organ injury by damping down the fibrogenic stimulus.