Article Publish Status: FREE
Abstract Title:

Preventive Effects of Carnosine on Lipopolysaccharide-induced Lung Injury.

Abstract Source:

Sci Rep. 2017 02 16 ;7:42813. Epub 2017 Feb 16. PMID: 28205623

Abstract Author(s):

Ken-Ichiro Tanaka, Toshifumi Sugizaki, Yuki Kanda, Fumiya Tamura, Tomomi Niino, Masahiro Kawahara

Article Affiliation:

Ken-Ichiro Tanaka


Acute respiratory distress syndrome (ARDS) is a potentially devastating form of acute lung injury, which involves neutrophilic inflammation and pulmonary cell death. Reactive oxygen species (ROS) play important roles in ARDS development. New compounds for inhibiting the onset and progression of ARDS are required. Carnosine (β-alanyl-L-histidine) is a small di-peptide with numerous activities, including antioxidant effects, metal chelation, proton buffering capacity and the inhibition of protein carbonylation and glycoxidation. We have examined the preventive effects of carnosine on tissue injury, oedema and inflammation in a murine model for ARDS. Oral administration of carnosine suppressed lipopolysaccharide (LPS)-induced vascular permeability, tissue injury and inflammation in the lung. In vivo imaging analysis revealed that LPS administration increased the level of ROS and that this increase was inhibited bycarnosine administration. Carnosine also suppressed LPS-induced neutrophilic inflammation (evaluated by activation of myeloperoxidase in the lung and increased extracellular DNA in bronchoalveolar lavage fluid). Furthermore, carnosine administration suppressed the LPS-induced endoplasmic reticulum stress response in vivo. These results suggest that the oral administration of carnosine suppresses LPS-induced lung injury via carnosine's ROS-reducing activity. Therefore, carnosine may be beneficial for suppressing the onset and progression of ARDS.

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