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Background and aims <p>Acute liver failure (ALF) is a rapidly progressing clinical syndrome with a high mortality rate and limited treatment options. In this study, we used the RIP1 kinase inhibitor necrostatin-1 (Nec-1) to explore the effect and mechanism of RIP1 in lipopolysaccharide (LPS)/D-galactosamine (GalN)-induced ALF.</p> Results <p>Nec-1 pretreatment significantly ameliorated ALF, as evidenced by reduced hepatic necrosis and serum alanine aminotransferase levels. Additionally, Nec-1 administration alleviated LPS/GalN-induced hepatocyte apoptosis in liver tissues. Further in vitro experiments revealed that Nec-1 inhibited the secretion of TNF-α from macrophages and reduced TNF-α-induced hepatocyte apoptosis.</p> Conclusions <p>Inhibition of RIP1 effectively alleviated LPS/GalN-induced ALF by reducing hepatic apoptosis and attenuating the secretion of TNF-α from macrophages, suggesting its potential as a therapeutic agent for ALF patients.</p>

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Inhibition RIP1 prevents acute liver failure by suppressing hepatic apoptosis and attenuating the secretion of TNF-α from macrophages

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月26日

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  • Aichun Li,
  • Dahua Chen,
  • Jianwei Shen

摘要

Background and aims

Acute liver failure (ALF) is a rapidly progressing clinical syndrome with a high mortality rate and limited treatment options. In this study, we used the RIP1 kinase inhibitor necrostatin-1 (Nec-1) to explore the effect and mechanism of RIP1 in lipopolysaccharide (LPS)/D-galactosamine (GalN)-induced ALF.

Results

Nec-1 pretreatment significantly ameliorated ALF, as evidenced by reduced hepatic necrosis and serum alanine aminotransferase levels. Additionally, Nec-1 administration alleviated LPS/GalN-induced hepatocyte apoptosis in liver tissues. Further in vitro experiments revealed that Nec-1 inhibited the secretion of TNF-α from macrophages and reduced TNF-α-induced hepatocyte apoptosis.

Conclusions

Inhibition of RIP1 effectively alleviated LPS/GalN-induced ALF by reducing hepatic apoptosis and attenuating the secretion of TNF-α from macrophages, suggesting its potential as a therapeutic agent for ALF patients.