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Chlorogenic acid protects mice against lipopolysaccharide-induced acute lung injury
Authors:Xu Zhang  Tingting Yang  Jianhua Shan  Lan Luo
Affiliation:a State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, 22 Hankou Rd, Nanjing, Jiangsu 210093, PR China
b Jiangsu Province Key Laboratory for Molecular, Medicine Biotechnology, College of Life Science, Nanjing Normal University, Nanjing 210046, PR China
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.
Keywords:CGA, chlorogenic acid   LPS, lipopolysaccharide   ALI, acute lung injury   ARDS, acute respiratory distress syndrome   MPO, myeloperoxidase   iNOS, inducible nitric oxide synthesis   NO, nitric oxide   PMNs, polymorphonuclear neutrophils   BALF, bronchoalveolar lavage fluid   TNF-α, tumor necrosis factor-α   IL-1, interleukin-1   IL-6, interleukin-6   PGE2, prostaglandin E2   DMSO, dimethyl sulfoxide   DEX, dexamethasone
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