Objective To observe the effects on the expression of tumour necrosis factor-α in hepatic fibrosis of rats after intervention of the renin-angiotensin-aldosterone system at different links. Methods Fifty SD rats were randomly divided into control group, model group and three treatment groups (captopril group, losartan group and spironolactone group), with 10 rats in each group. The rats in the control group were subcutaneously injected with olive oil, and the rats in the other groups were subcutaneously injected with 40% CCL4. From the second day, the three treatment groups were treated with captopril 60 mg/kg, losartan 10 mg/kg and spironolactone 100 mg/kg, respectively, and the model group and the control group were given the same amount of normal saline, once a day. The rats were sacrificed at the 8th week, and the expression of tumor necrosis factor-α mRNA in rat liver tissue was detected by RealTime-PCR. Pathological staining was used to observe the pathological changes of rat liver tissue. Results There was significant difference in liver fiber area among the three treatment groups (P <0.05). There were significant differences in liver fiber area between the three treatment groups and the model group (P <0.05). The liver fiber area of rats in the control group and the three treatment groups was lower than that in the model group, and the difference was statistically significant (P <0.05). There was no significant difference in the expression of TNF-α mRNA in liver tissue among the three treatment groups (P >0.05). The expression of TNF-α mRNA in liver tissue of the three treatment groups was lower than that of the model group, and the difference was statistically significant (P <0.05). The expression of TNF-α mRNA in the liver tissue of the model group and the three treatment groups was higher than that of the control group, and the difference was statistically significant (P <0.05). Conclusion Intervention in different links of RAAS system can inhibit the formation of hepatic fibrosis, which may be related to the inhibition of tumor necrosis factor-α expression.