An Italian study tested whether the administration of curcumin limits fibrogenic evolution in a murine model of nonalcoholic steatohepatitis. They demonstrated that curcumin decreased the intrahepatic gene expression of monocyte chemoattractant protein-1, CD11b, procollagen type I, and tissue inhibitor of metalloprotease (TIMP)-1, together with protein levels of alpha-smooth muscle actin, a marker of fibrogenic cells. In addition, curcumin reduced the generation of reactive oxygen species in cultured HSCs and inhibited the secretion of TIMP-1 both in basal conditions and after the induction of oxidative stress. This study so proposed that curcumin administration effectively limits the development and progression of fibrosis in mice with experimental steatohepatitis and reduces TIMP-1 secretion and oxidative stress in cultured stellate cells [44] .