Abstract
Models created by the intraperitoneal injection of lipopolysaccharide (LPS) and D-galactosamine (D-GalN) have been widely used to study the pathogenesis of human acute liver failure (ALF) and drug development. Our previous study reported that oyster (Crassostrea gigas) hydrolysate (OH) had a hepatoprotective effect in LPS/D-GalN-injected mice. This study was performed to identify the hepatoprotective effect of the tyrosine-alanine (YA) peptide, the main component of OH, in a LPS/D-GalN-injected ALF mice model. We analyzed the effect of YA on previously known mechanisms of hepatocellular injury in the model. LPS/D-GalN-injected mice showed inflammatory, apoptotic, ferroptotic, and pyroptotic liver injury. The pre-administration of YA (10 mg/kg or 50 mg/kg) significantly reduced the liver damage factors. The hepatoprotective effect of YA was higher in the 50 mg/kg YA pre-administered group than in the 10 mg/kg YA pre-administered group. These results showed that YA had a hepatoprotective effect by reducing inflammation, apoptosis, ferroptosis, and pyroptosis in the LPS/D-GalN-injected ALF mouse model. We suggest that YA can be used as a functional peptide for the prevention of acute liver injury.
Highlights
The acute liver failure (ALF) model was generated by the intraperitoneal injection of LPS (1 μg/kg) and D-galactosamine
Body weight was measured at the beginning and end of the experiment, and liver weight was measured immediately after sacrificing the mice
Previously knownLPS/D-GalN-inmechanisms of hepato jected miceasused as an model in this study are referred to as models forfulminant fulminant mice used an model in this study are referred to as models for lular damage in a mouse model capable of mimicking ALF
Summary
Acute liver failure (ALF) is the most common life-threatening disease in adults without pre-existing liver disease, and it mainly occurs in the 30s [1]. There are many causes of ALF that include hepatitis, acetaminophen overdose, toxins, autoimmune diseases, Wilson’s disease, and unknown factors. Herbal supplements cannot be free from triggers of ALF [2]. Since there are few effective treatments for ALF other than liver transplantation, studies to find strategies for the treatment and prevention of ALF using experimental animal models are continuously being performed. In the early stages of ALF, the incidence of bacterial infection is high [3,4], which might aggravate the clinical condition and prognosis [5]. An uncontrolled inflammatory response impairs the liver’s defenses and causes massive cell death of hepatocytes, leading to acute liver damage and severe
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