Publication: Neoastilbin ameliorates sepsis-induced liver and kidney injury by blocking the TLR4/NF-κB pathway
Authors
Xu, Ruiming ; Wang, Dawei ; Shao, Zhengyi ; Li, Xiangbo ; Cao, Qiumei
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Publisher
Universidad de Murcia. Departamento de Biología Celular e Histología
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DOI
https://doi.org/10.14670/HH-18-719
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info:eu-repo/semantics/article
Description
Abstract
Sepsis frequently causes systemic
inflammatory response syndrome and multiple organ
failure in patients. Neoastilbin (NAS) is a flavonoid that
plays vital functions in inflammation. This work aims to
investigate the protective effects of NAS against sepsisinduced liver and kidney injury and elucidate its
underlying mechanisms. The mouse model was
established using cecal ligation puncture (CLP)
induction. NAS was given to mice by gavage for 7
consecutive days before surgery. Liver and kidney
function, oxidative stress, and inflammatory factors in
serum or tissues were examined by ELISA or related
kits. The expression of relevant proteins was assessed by
Western blot. Hematoxylin and eosin and/or periodic
acid-Schiff staining revealed that NAS ameliorated the
pathological damage in liver and kidney tissues of CLPinduced mice. NAS improved liver and kidney
functions, as evidenced by elevated levels of blood urea
nitrogen, Creatinine, ALT, and AST in the serum of
septic mice. TUNEL assay and the expression of Bcl-2
and Bax showed that NAS dramatically reduced
apoptosis in liver and renal tissues. NAS treatment
lowered the levels of myeloperoxidase and
malondialdehyde, while elevated the superoxide
dismutase content in liver and kidney tissues of CLPinduced mice. The levels of inflammatory cytokines (IL6, TNF-α, and IL-1β) in the serum and both tissues of
CLP-injured mice were markedly decreased by NAS.
Mechanically, NAS downregulated TLR4 expression
and inhibited NF-κB activation, and overexpression of
TLR4 reversed the protective effects of NAS against
liver and kidney injury. Collectively, NAS attenuated
CLP-induced apoptosis, oxidative stress, inflammation,
and dysfunction in the liver and kidney by restraining
the TLR4/NF-κB pathway.
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