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Protective effect of cinnamic acid in endotoxin‐poisoned mice
Author(s) -
Xu Feng,
Wang Feng,
Wen Taoqun,
Sang Wentao,
He Xinyu,
Li Ling,
Zeng Nan
Publication year - 2017
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.5944
Subject(s) - lipopolysaccharide , inflammasome , spleen , tumor necrosis factor alpha , lung , pyrin domain , pharmacology , caspase 1 , tlr4 , immunology , receptor , proinflammatory cytokine , chemistry , medicine , inflammation
In this work, we aimed to evaluate the protective effect of cinnamic acid (CD) on lipopolysaccharide (LPS; Escherichia coli 055:B5)‐induced endotoxin‐poisoned mice and clarify the underlying mechanisms. The mice were administrated CD 5 d before 15 mg/kg LPS challenge. 12 hr later, thymus was separated for determination of thymus indexes. Lung and spleen tissues were collected for histologic examination and the wet/dry weight ratio of lung was calculated, and serum was acquired for tumor necrosis factor‐α (TNF‐α), interleukin (IL)‐18, and IL‐1β measurement. Moreover, the expression of NOD‐like receptor (NLR) family, pyrin domain‐containing 3 (NLRP3) inflammasome was determined in lung. CD increased the thymus indexes and decreased lung wet/dry weight ratio. In addition, CD improved the lung and spleen histopathological changes induced by LPS and decreased the number of neutrophils in lung tissues. CD also inhibited the pro‐inflammatory cytokines (TNF‐α, IL‐18, and IL‐1β) production in serum. Furthermore, CD suppressed the LPS‐induced NLRP3, Caspase‐1, and IL‐1β mRNA expression in lung, as well as the expression of NLRP3 and Caspase‐1 (p20) protein. CD may have protective effects in endotoxin‐poisoned mice via inhibiting the activation of NLRP3 inflammasome, and can be considered as a potential therapeutic candidate for diseases involved in endotoxin poisoning such as sepsis.