AIM:To study the expression of peroxisome proliferatoractivated receptor-γ(PPARγ) in the liver of rats with fattyliver disease (FLD) and to explore the role of PPARγ in thepathogenesis of FLD to provide the basis for using PPARγligand to treat patients with FLD.METHODS:Forty Wistar rats were divided into 4 groupsof ten rats each randomly:normal group (group A),alcoholgroup (group B),fat-rich diet group (group C),alcohol andfat-rich diet group (group D).The rats were sacrificed atthe end of the 16th week from the feeding day.Alanineaminotransferase (ALT),tumor necrosis factor-alfa (TNFα)in serum and malondialdehyde (MDA) in liver homogenatewere determined;livers were collected for observingpathologic changes by HE,Sudan Ⅳ,Masson stain undermicroscope.The morphologic results were analyzed bypicture quantitative analysis technique.The changes ofultrastructure were also examined under electron microscope.The expression of PPARγ in liver was detected by immunoh-istochemistry and RT-PCR.The correlations between theexpression of PPARy and biochemical indexes,and liverhistology were analyzed.RESULTS:The steatosis,inflammation,necrosis and fibrosiswere present in livers of different experimental groups,especially in livers of alcohol and fat-rich diet group.Thecontent of immunodetectable PPARγ was decreasedremarkably in the livers of model rats (group B-D);the levelin alcohol and fat-rich diet group (3.43±1.48) was significantlylower than that in normal group (18.34±3.73),alcohol group(8.82±2.52) and fat-rich diet group (11.73±2.51) (all P<0.01).The level of PPARγ mRNA was also lower in the livers ofmodel rats (group B-D) than in livers of controls.Theexpression of PPARγ in rat liver correlated negatively withthe degree of its inflammation,necrosis and fibrosis,aswell as the level of serum TNFα and the content of MDA inliver homogenates,but not with steatosis or serum ALT.CONCLUSION:Decreased expression of PPARγ may playan important role in the development of hepatocellularinflammation,necrosis and fibrosis of rats with FLD.Thus,activating PPARγ by its ligand can be anticipated to providea therapy target for FLD. AIM: To study the expression of peroxisome proliferator activated receptor-γ (PPARγ) in the liver of rats with fattyliver disease (FLD) and to explore the role of PPARγ in the pathogenesis of FLD to provide the basis for using PPARγligand to treat patients with FLD. METHODS: Forty Wistar rats were divided into 4 groups of ten rats each randomly: normal group (group A), alcohol group (group B), fat-rich diet group (group C), alcohol and fat-rich diet group Rats were sacrificed atthe end of the 16th week from the feeding day. Alanine aminotransferase (ALT), tumor necrosis factor-alfa (TNFα) in serum and malondialdehyde (MDA) in liver homogenate determined; livers were collected for observingpathologic changes by HE, Sudan IV , Masson stain undermicroscope. The morphologic results were analyzed by image quantitative analysis technique. The changes ofultrastructures were also examined under electron microscope. The expression of PPARγ in liver was detected by immunoh-istochemistry and RT- PCR. The correlations between the expression of PPARy and biochemical indexes, and liver histology were analyzed .RESULTS: The steatosis, inflammation, necrosis and fibrosiswere present in livers of different experimental groups, especially in livers of alcohol and fat-rich diet group. Content of immunodetectable The level of alcohol and fat-rich diet group (3.43 ± 1.48) was significantly lower than those in normal group (18.34 ± 3.73), alcohol group (8.82 ± 2.52) and fat -rich diet group (11.73 ± 2.51) (all P <0.01). The level of PPARγ mRNA was also lower in the livers of mice model group (group BD) than in livers of controls. The expression of PPARγ in rat liver correlated negatively with the degree of its inflammation, necrosis and fibrosis, aswell as the level of serum TNFα and the content of MDA inliver homogenates, but not with steatosis or serum ALT. CONCLUSION: Decreased expression of PPARγ may playan important role in the development o f hepatocellularinflammation, necrosis and fibrosis of rats with FLD.Thus, activating PPARγ by its ligand can be anticipated to providea therapy target for FLD.