Oyster-Derived Tyr-Ala (YA) Peptide Prevents Lipopolysaccharide/D-Galactosamine-Induced Acute Liver Failure by Suppressing Inflammatory, Apoptotic, Ferroptotic, and Pyroptotic Signalsopen access
- Siregar, Adrian S.; Nyiramana, Marie Merci; Kim, Eun-Jin; Cho, Soo Buem; Woo, Min Seok; Lee, Dong Kun; Hong, Seong-Geun; Han, Jaehee; Kang, Sang Soo; Kim, Deok Ryong; Choi, Yeung Joon; Kang, Dawon
- Issue Date
- acute liver injury; apoptosis; ferroptosis; inflammation; oyster; peptide; pyroptosis
- MARINE DRUGS, v.19, no.11
- Journal Title
- MARINE DRUGS
- 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.
- Files in This Item
- There are no files associated with this item.
- Appears in
- College of Medicine > Department of Medicine > Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.