Abstract
Acute liver failure is a fatal syndrome attributed to massive hepatocyte apoptosis that is resistant to conventional medical therapies. Consequently, liver transplantation is required in many cases. An experimental liver failure model induced by galactosamine (Gal) and lipopolysaccharide (LPS) mimics clinical acute liver failure. In this model, LPS stimulates macrophages to release TNFα, which induces apoptosis in Gal-sensitized hepatocytes, causing acute liver failure. Hydrogen sulphide (H2S), which is an endogenously produced gaseous signaling molecule, has anti-apoptotic as well as anti-inflammatory properties. Previously, we reported that H2S attenuates liver dysfunction arising from LPS-induced systemic inflammation [1]. It has also been reported that H2S reduces hepatic ischemia/reperfusion injury by inhibition of apoptosis in the liver [2]. However, it is still unknown whether H2S exerts hepatoprotective effects against acute liver failure, in which both inflammatory responses and apoptosis have critical roles. Here, we examined the impact of H2S on acute liver failure in mice induced by Gal and LPS.
Highlights
Acute liver failure is a fatal syndrome attributed to massive hepatocyte apoptosis that is resistant to conventional medical therapies
H2S inhalation after Gal/LPS challenge further augmented phosphorylation of STAT3 compared to air alone
The protective effects of H2S inhalation after Gal/LPS challenge were associated with upregulation of gene expression of antiinflammatory IL-10, which stimulates STAT3 phosphorylation, in the liver
Summary
Acute liver failure is a fatal syndrome attributed to massive hepatocyte apoptosis that is resistant to conventional medical therapies. An experimental liver failure model induced by galactosamine (Gal) and lipopolysaccharide (LPS) mimics clinical acute liver failure. In this model, LPS stimulates macrophages to release TNFa, which induces apoptosis in Gal-sensitized hepatocytes, causing acute liver failure. It has been reported that H2S reduces hepatic ischemia/reperfusion injury by inhibition of apoptosis in the liver [2]. It is still unknown whether H2S exerts hepatoprotective effects against acute liver failure, in which both inflammatory responses and apoptosis have critical roles. We examined the impact of H2S on acute liver failure in mice induced by Gal and LPS
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