The present study aimed to investigate the effects of endogenous
hydrogen sulfide (H2S) on the expression levels of
angiotensin II type 1 receptor (AGTR1) in a rat model of
carbon tetrachloride (CCl4)‑induced hepatic
fibrosis. A total of 56 Wistar rats were randomly divided into four groups: Normal control group, model group,
sodium hydrosulfide (
NaHS) group, and DL‑propargylglycine (PAG) group. Hepatic
fibrosis was induced by CCl4. The rats in the PAG group were intraperitoneally injected with PAG, an inhibitor of cystathionine‑γ‑lyase (CSE). The rats in the
NaHS group were intraperitoneally injected with
NaHS. An equal volume of
saline solution was intraperitoneally injected into both the control and model groups. All rats were sacrificed at week three or four following treatment. The serum levels of
hyaluronidase (HA),
laminin protein (LN),
procollagen III (PcIII), and
collagen IV (cIV) were detected using ELISA. The serum levels of
alanine transaminase (ALT),
aspartate transaminase (AST), and
albumin (ALB) were detected using an automatic biochemical analyzer. The liver
mRNA expression levels of CSE were detected by reverse transcription‑quantitative polymerase chain reaction. The liver expression levels of AGTR1 and the plasma expression levels of H2S were detected using western blot analyses. The results indicated that the severity of hepatic
fibrosis, the serum expression levels of HA, LN, PcIII, cIV, ALT, and AST, the liver expression levels of CSE and AGTR1, and the plasma expression levels of H2S were significantly higher in the PAG group, as compared with the model group (P<0.05). Conversely, the expression levels of ALB were significantly lower in the PAG group, as compared with the model group. In addition, the severity of hepatic
fibrosis, the serum expression levels of HA, LN, PcIII, cIV, ALT, and AST, the liver expression levels of CSE and AGTR1, and the plasma expression levels of H2S were significantly lower in the
NaHS group, as compared with the model group (P<0.05). These results suggest that endogenous H2S is associated with CCl4‑induced hepatic
fibrosis in rats, and may exhibit anti‑fibrotic effects. Furthermore, H2S reduced the liver expression levels of AGTR1, which may be associated with the delayed progression of hepatic
fibrosis.