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Chlorogenic acid protects mice against lipopolysaccharide-induced acute lung injury.

Abstract
Chlorogenic acid (CGA) is one of the most abundant polyphenol compounds in human diet. Our previous in vitro study demonstrates that CGA presents anti-inflammatory activities in RAW 264.7 cells. Here we show that CGA protects mice against lipopolysaccharide (LPS)-induced acute lung injury (ALI). We treated mice with CGA (5, 20 and 50 mg/kg body weight) 30 min or 3 h after intratracheal administration of LPS. The histological results showed that CGA, at dose of 50 mg/kg, protected mice from LPS-induced ALI which displayed by edema, haemorrhage, blood vessel and alveolar structural damage. CGA inhibited LPS-increased pulmonary MPO activity and migration of polymorphonuclear neutrophils (PMNs) into bronchoalveolar lavage fluid (BALF). Furthermore, CGA markedly decreased the activity of inducible nitric oxide synthase (iNOS) in lung tissues and thus prevented nitric oxide (NO) release in response to LPS challenge. In conclusion, these results indicated that CGA was greatly effective in inhibiting ALI and might act as a potential therapeutic reagent for treating ALI in the future.
AuthorsXu Zhang, Huang Huang, Tingting Yang, Yin Ye, Jianhua Shan, Zhimin Yin, Lan Luo
JournalInjury (Injury) Vol. 41 Issue 7 Pg. 746-52 (Jul 2010) ISSN: 1879-0267 [Electronic] Netherlands
PMID20227691 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Copyright2010 Elsevier Ltd. All rights reserved.
Chemical References
  • Anti-Inflammatory Agents
  • Chlorogenic Acid
  • Peroxidase
  • Nitric Oxide Synthase Type II
Topics
  • Acute Lung Injury (chemically induced, pathology, prevention & control)
  • Animals
  • Anti-Inflammatory Agents (administration & dosage, pharmacology)
  • Chlorogenic Acid (administration & dosage, pharmacology)
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Drug Evaluation, Preclinical
  • Lung (enzymology, pathology)
  • Male
  • Mice
  • Mice, Inbred ICR
  • Nitric Oxide Synthase Type II (metabolism)
  • Peroxidase (metabolism)

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