Open AccessJuniperus communis extract ameliorates lipopolysaccharide‐induced acute kidney injury through the adenosine monophosphate–activated protein kinase pathway
Author(s) -
Lin TaChin,
Lu ChiaWen,
Chang KaiFu,
Lee ChungJen
Publication year - 2022
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/fsn3.2941
Subject(s) - ampk , lipopolysaccharide , heme oxygenase , oxidative stress , pharmacology , kidney , adenosine monophosphate , protein kinase a , cyclic adenosine monophosphate , acute kidney injury , tumor necrosis factor alpha , nf κb , antioxidant , chemistry , keap1 , adenosine , inflammation , medicine , kinase , endocrinology , biochemistry , heme , enzyme , transcription factor , receptor , gene
Septic shock can aggravate organ dysfunction and even lead to death. Juniperus communis (JCo) extract has been experimentally demonstrated to have anti‐inflammatory and antioxidant effects. We investigated the anti‐inflammatory and antioxidant mechanism of JCo extract in vivo and in vitro. In a lipopolysaccharide (LPS)‐induced acute kidney injury rat model, JCo extract improved animal survival, reduced kidney injury scores, suppressed kidney injury molecule‐1, and preserved E‐cadherin expression from LPS damage, as demonstrated by the immunohistochemistry examinations of the rat kidneys. In LPS‐stimulated NRK‐52E cells, JCo extract inhibited nuclear factor‐κB (NF‐κB) and increased adenosine monophosphate–activated protein kinase (AMPK) expression, prompting the activation of the antioxidant nuclear factor erythroid 2–related factor‐2/heme oxygenase‐1 pathway against oxidative stress. JCo extract ameliorated LPS‐induced acute kidney injury by suppressing NF‐κB signaling and stimulating the release of tumor necrosis factor‐α and interleukin‐1β through the AMPK pathway.