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Protective effect of cinnamic acid in endotoxin-poisoned mice.

Authors
  • Xu, Feng1
  • Wang, Feng1
  • Wen, Taoqun1
  • Sang, Wentao1
  • He, Xinyu1
  • Li, Ling1
  • Zeng, Nan1
  • 1 Department of Pharmacology, College of Pharmacy, Chengdu University of TCM, Chengdu, Sichuan Province, China. , (China)
Type
Published Article
Journal
Phytotherapy Research
Publisher
Wiley (John Wiley & Sons)
Publication Date
Oct 11, 2017
Identifiers
DOI: 10.1002/ptr.5944
PMID: 29024091
Source
Medline
Keywords
License
Unknown

Abstract

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.

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