Open AccessSilkworm pupa oil attenuates acetaminophen‐induced acute liver injury by inhibiting oxidative stress‐mediated NF‐κB signaling
Author(s) -
Long Xingyao,
Song Jiajia,
Zhao Xin,
Zhang Yu,
Wang Hongwei,
Liu Xinqi,
Suo Huayi
Publication year - 2020
Publication title -
food science and nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.614
H-Index - 27
ISSN - 2048-7177
DOI - 10.1002/fsn3.1296
Subject(s) - acetaminophen , proinflammatory cytokine , oxidative stress , aspartate transaminase , alanine transaminase , liver injury , pharmacology , transaminase , medicine , glutathione , alanine aminotransferase , tumor necrosis factor alpha , chemistry , inflammation , biochemistry , enzyme , alkaline phosphatase
Acetaminophen (APAP) overdose causes severe hepatotoxicity and acute liver failure. The current study aims to investigate the protection effects of silkworm pupa oil (SPO) against acute hepatic injury in APAP‐exposed Kunming mice. Our results showed that the liver index and the levels of serum alanine transaminase (ALT) and aspartate transaminase (AST) in mice subjected to APAP treatment were decreased by SPO. Supplement of SPO also restored hepatic histopathological alterations induced by APAP. The APAP‐induced increase in proinflammatory cytokines, including TNF‐α, IL‐6, and IL‐12, was reversed by SPO, which was mediated by the reduction of nuclear factor (NF)‐κB p65 expression and the increase in the expression of IκB‐α in liver tissue. Moreover, SPO inhibited APAP‐triggered oxidative stress by decreasing MDA level and increasing the activities of SOD and GSH‐Px. Collectively, SPO attenuated hepatic injury induced by APAP, which attributed to the suppression of oxidative stress‐mediated NF‐κB signaling. Our findings suggest that SPO supplementation may be potential strategy against acute hepatic injury.