• Exogenous H₂S inhibits activated HSC-T6 cells and induces cell cycle arrest and apoptosis. Decreased Phospho-p38 and increased Phospho-Akt expressions may mediate the anti-fibrosis effect by exogenous H₂S in mice.1
  • Reduction of CSE expression in the liver with cirrhosis contributes to the development of increased intrahepatic resistance and portal hypertension. H₂S reduced portal pressure due to the administration of NE in mice.2
  • Local inhibition of endogenous hydrogen sulfide in atria has opposite effect in cirrhotic versus control rats demonstrating impaired chronotropic responsiveness to adrenergic stimulation.3
  • Exogenous hydrogen sulfide can effectively inhibit the development of hepatic fibrosis, reduce the expression of TGF-β1, and decrease the sediment of extracellular matrix in the liver tissues.4
  • Cysteine was markedly reduced in patients with compensated chronic liver disease and study suggests that a derangement in sulphur amino acid metabolism exists in humans with chronic liver disease.5)
  • H₂S protects the murine liver against I/R injury through an upregulation of intracellular antioxidant and antiapoptotic signaling pathways.6
  • NaHS ameliorated hepatic IRI by direct and indirect anti-oxidant activities by augmenting pro-survival, anti-apoptotic, and anti-inflammatory signals via mechanisms involving Nrf-2, and by accelerating hepatic regeneration via mechanisms involving Akt-p70S6k.7
  • A number of in vivo and in vitro studies have shown that both endogenous H₂S level and the expressions of H₂S -generating enzymes in plasma and tissues are significantly downregulated during fibrosis. Supplement with exogenous H₂S mitigates the severity of fibrosis in various experimental animal models. The protective role of H₂S in the development of fibrosis is primarily attributed to its antioxidation, antiapoptosis, anti-inflammation, proangiogenesis, and inhibition of fibroblasts activities.8
  • Results for the first time demonstrated that H₂S could reduce serum TG level and ameliorate NAFLD by activating liver autophagy via the AMPK-mTOR pathway.9