Oyster-Derived Tyr-Ala (YA) Peptide Prevents Lipopolysaccharide/D-Galactosamine-Induced Acute Liver Failure by Suppressing Inflammatory, Apoptotic, Ferroptotic, and Pyroptotic Signals
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 hepatop...
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2021
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oai:doaj.org-article:a748721d4c68402dbc1cf018aac77e112021-11-25T18:12:50ZOyster-Derived Tyr-Ala (YA) Peptide Prevents Lipopolysaccharide/D-Galactosamine-Induced Acute Liver Failure by Suppressing Inflammatory, Apoptotic, Ferroptotic, and Pyroptotic Signals10.3390/md191106141660-3397https://doaj.org/article/a748721d4c68402dbc1cf018aac77e112021-10-01T00:00:00Zhttps://www.mdpi.com/1660-3397/19/11/614https://doaj.org/toc/1660-3397Models 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.Adrian S. SiregarMarie Merci NyiramanaEun-Jin KimSoo Buem ChoMin Seok WooDong Kun LeeSeong-Geun HongJaehee HanSang Soo KangDeok Ryong KimYeung Joon ChoiDawon KangMDPI AGarticleacute liver injuryapoptosisferroptosisinflammationoysterpeptideBiology (General)QH301-705.5ENMarine Drugs, Vol 19, Iss 614, p 614 (2021) |
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acute liver injury apoptosis ferroptosis inflammation oyster peptide Biology (General) QH301-705.5 |
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acute liver injury apoptosis ferroptosis inflammation oyster peptide Biology (General) QH301-705.5 Adrian S. Siregar Marie Merci Nyiramana Eun-Jin Kim Soo Buem Cho Min Seok Woo Dong Kun Lee Seong-Geun Hong Jaehee Han Sang Soo Kang Deok Ryong Kim Yeung Joon Choi Dawon Kang Oyster-Derived Tyr-Ala (YA) Peptide Prevents Lipopolysaccharide/D-Galactosamine-Induced Acute Liver Failure by Suppressing Inflammatory, Apoptotic, Ferroptotic, and Pyroptotic Signals |
description |
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. |
format |
article |
author |
Adrian S. Siregar Marie Merci Nyiramana Eun-Jin Kim Soo Buem Cho Min Seok Woo Dong Kun Lee Seong-Geun Hong Jaehee Han Sang Soo Kang Deok Ryong Kim Yeung Joon Choi Dawon Kang |
author_facet |
Adrian S. Siregar Marie Merci Nyiramana Eun-Jin Kim Soo Buem Cho Min Seok Woo Dong Kun Lee Seong-Geun Hong Jaehee Han Sang Soo Kang Deok Ryong Kim Yeung Joon Choi Dawon Kang |
author_sort |
Adrian S. Siregar |
title |
Oyster-Derived Tyr-Ala (YA) Peptide Prevents Lipopolysaccharide/D-Galactosamine-Induced Acute Liver Failure by Suppressing Inflammatory, Apoptotic, Ferroptotic, and Pyroptotic Signals |
title_short |
Oyster-Derived Tyr-Ala (YA) Peptide Prevents Lipopolysaccharide/D-Galactosamine-Induced Acute Liver Failure by Suppressing Inflammatory, Apoptotic, Ferroptotic, and Pyroptotic Signals |
title_full |
Oyster-Derived Tyr-Ala (YA) Peptide Prevents Lipopolysaccharide/D-Galactosamine-Induced Acute Liver Failure by Suppressing Inflammatory, Apoptotic, Ferroptotic, and Pyroptotic Signals |
title_fullStr |
Oyster-Derived Tyr-Ala (YA) Peptide Prevents Lipopolysaccharide/D-Galactosamine-Induced Acute Liver Failure by Suppressing Inflammatory, Apoptotic, Ferroptotic, and Pyroptotic Signals |
title_full_unstemmed |
Oyster-Derived Tyr-Ala (YA) Peptide Prevents Lipopolysaccharide/D-Galactosamine-Induced Acute Liver Failure by Suppressing Inflammatory, Apoptotic, Ferroptotic, and Pyroptotic Signals |
title_sort |
oyster-derived tyr-ala (ya) peptide prevents lipopolysaccharide/d-galactosamine-induced acute liver failure by suppressing inflammatory, apoptotic, ferroptotic, and pyroptotic signals |
publisher |
MDPI AG |
publishDate |
2021 |
url |
https://doaj.org/article/a748721d4c68402dbc1cf018aac77e11 |
work_keys_str_mv |
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