AIM:To observe the possible effects of transforming growthfactor (TGF) β_1,interleukin (IL)-6,tumor-necrosis factor(TNF) α and IL-10 on experimental rat hepatic fibrosis.METHODS:One hundred SD rats were divided randomlyinto the three groups.Control group received intraperitonealinjection of saline (2ml·kg~(-1)),twice a week.Fibrogenesisgroup was injected intraperitoneally with 50% carbontetrachloride (CCl_4) (2ml·kg~(-1)) twice a week.Fibrosis-intervention group was given IL-10 at a dose of 4μg·kg~(-1)20 minutes before CCl_4 administration from the third week.At the fifth,seventh,and ninth weeks,7 to 10 rats in eachgroup were sacrificed to collect serum.Levels of TGF-β_1,TNF-α,IL-6 and IL-10 were determined by enzyme-linkedimmunosorbent assay (ELISA).The liver tissues were takenfor routine histological examination.RESULTS:Hepatic fibrosis was developed with the injectionof CCl_4.Values of the circulating TGFβ_1,TNFα,IL-6 and IL-10 in the control group were 25.49±5.56 ng·L~(-1),15.18±3.83ng·L~(-1),63.64±13.03 ng·L~(-1) and 132.90±12.13 ng·L~(-1),respectively.Their levels in the CCl_4-intoxication group were31.13±6.41 ng·L~(-1),18.91±5.31 ng·L~(-1),89.08±25.39 ng·L~(-1) and57.63±18.88 ng·L~(-1),respectively,and those in the IL-10-intervention group were 26.11±5.32 ng·L~(-1),13.99±1.86 ng·L~(-1),74.71±21.15 ng·L~(-1) and 88.19±20.81 ng·L~(-1),respectively.Agradual increase was observed in the levels of TGFβ_1,TNFαand IL-6 during hepatic fibrogenesis.These changes werepartially reversed by simultaneous administration of IL-10.Thehistological parameters,characterized by CCl_4-intoxification,also seemed to be improved with IL-10 treatment,the collagenproduction was reduced at the ninth week and the histologicalactivity index was decreased from 7.9±1.2 to 4.7±0.9.CONCLUSION:TGFβ_1,TNFα and IL-6 may play importantroles during CCl_4-induced hepatic fibrogenesis,and IL-10may counterbalance their effects. AIM: To observe the possible effects of transforming growth factor (TGF) β_1, interleukin (IL) -6, tumor-necrosis factor (TNF) α and IL-10 on experimental rat hepatic fibrosis.METHODS: One hundred SD rats were divided randomly three groups. Control group received intraperitonealjection of saline (2 ml · kg -1) twice twice a week. Fibrogenesis group was injected intraperitoneally with 50% carbon tetrachloride (CCl 4) (2 ml · kg -1) twice a week. -intervention group was given IL-10 at a dose of 4 μg · kg -1 (for 20 minutes before CCl_4 administration from the third week. At the fifth, seventh, and ninth weeks, 7 to 10 rats in each group were sacrificed to collect serum.Levels of TGF-β_1, TNF-α, IL-6 and IL-10 were determined by enzyme-linked immunosorbent assay (ELISA). The liver tissues were taken for routine histological examination.RESULTS: Hepatic fibrosis was developed with the injection of CCl_4. Values ​​of the circulating TGFβ_1, TNFα, IL-6 and IL-10 in the control group were 25.49 ± 5.56 ng · L ~ ( -1, 15.18 ± 3.83 ng · L -1, 63.64 ± 13.03 ng · L -1 and 132.90 ± 12.13 ng · L -1, respectively.Their levels in the CCl 4 -intxication group were 31.13 ± 6.41 ng · L -1, 18.91 ± 5.31 ng · L -1, 89.08 ± 25.39 ng · L -1 and57.63 ± 18.88 ng · L -1, respectively. , respectively, and those in the IL-10-intervention group were 26.11 ± 5.32 ng · L -1, 13.99 ± 1.86 ng · L -1, 74.71 ± 21.15 ng · L -1 and 88.19 ± 20.81 ng · L -1, respectively. Agradual increase was observed in the levels of TGFβ_1, TNFα and IL-6 during hepatic fibrogenesis. These changes were partized vectorially reversed by administration of IL-10. Thehistological parameters, characterized by CCl_4 -intoxification, also seemed to be improved with IL-10 treatment, the collagen production was reduced at the ninth week and the histologicalactivity index was decreased from 7.9 ± 1.2 to 4.7 ± 0.9. CONCLUSION: TGFβ_1, TNFα and IL-6 may play importantroles during CCl_4-induced hepatic fibrogenesis, and IL-10may counterbalance their effects.