Table 1.
Experimental models | Effects | Proposed mechanisms | Refs. |
---|---|---|---|
Hepatic fibrosis in vivo (rat) | NaHS (56 μmol/kg/day) attenuates CCl4-induced hepatic fibrosis | Reduction of liver expression levels of AGTR1 | [20] |
Hepatic fibrosis in vivo (rat) | NaHS solution (10 mmol/kg body weight) shows protective effects on CCl4-induced hepatic fibrosis | Decreased expression of p38 and increased expression of phospho-Akt | [88] |
Hepatic fibrosis in vivo (rat) | NaHS solution (10 mmol/kg body weight) attenuates CCl4-induced hepatic fibrosis and ECM expression | Induction of cell cycle arrest and apoptosis in activated hepatic stellate cells | [89] |
Hepatic fibrosis in vivo (rat) | NaHS (56 μmol/kg/day) attenuates CCl4-induced hepatic fibrosis | Reduction of the expression of TGF-β1 and sediment of ECM in the liver tissues | [90] |
Hepatic fibrosis in vitro (rat) | DATS (an H2S donor, 10 μM) reduces H2O2-induced upexpression of fibrotic protein in HSCs | Unknown | [91] |
CCl4: carbon tetrachloride; AGTR1: angiotensin II type 1 receptor; TGF-β1: transforming growth factor-β1; H2O2: hydrogen peroxide.