astaxanthine and Pneumonia

astaxanthine has been researched along with Pneumonia* in 1 studies

Other Studies

1 other study(ies) available for astaxanthine and Pneumonia

Article	Year
Astaxanthin suppresses cigarette smoke and lipopolysaccharide-induced airway inflammation through induction of heme oxygenase-1. Cellular and molecular biology (Noisy-le-Grand, France), 2019, Jan-31, Volume: 65, Issue:1 The present study was carried out to evolve an effective treatment strategy for chronic obstructive pulmonary disease (COPD). Astaxanthin (AS) is abundantly present in red pigments of crustaceans, and has also been proven to have considerable biological activities. The anti-inflammatory effect of AS was evaluated in lipopolysaccharide (LPS)-exposed RAW264.7 macrophages. It was found that AS markedly inhibited elevation of NO and pro-inflammatory mediators. Moreover, it downregulated iNOS in LPS-stimulated RAW264.7 cells, suppressed the release of pro-inflammatory cytokines, and decreased ROS levels in mice exposed to cigarette smoke (CS) and LPS. These results imply that AS has therapeutic and prophylactic potential in the airway inflammatory response associated with COPD. Topics: Animals; Bronchoalveolar Lavage Fluid; Cell Death; Cell Survival; Cytokines; Disease Models, Animal; Enzyme Induction; Heme Oxygenase-1; Inflammation Mediators; Lipopolysaccharides; Lung; Macrophages; Male; Mice; Mice, Inbred C57BL; Neutrophils; Nitric Oxide; Nitric Oxide Synthase Type II; Pneumonia; RAW 264.7 Cells; Reactive Oxygen Species; RNA, Messenger; Smoking; Xanthophylls	2019

Article

Year

Astaxanthin suppresses cigarette smoke and lipopolysaccharide-induced airway inflammation through induction of heme oxygenase-1.

Cellular and molecular biology (Noisy-le-Grand, France), 2019, Jan-31, Volume: 65, Issue:1

The present study was carried out to evolve an effective treatment strategy for chronic obstructive pulmonary disease (COPD). Astaxanthin (AS) is abundantly present in red pigments of crustaceans, and has also been proven to have considerable biological activities. The anti-inflammatory effect of AS was evaluated in lipopolysaccharide (LPS)-exposed RAW264.7 macrophages. It was found that AS markedly inhibited elevation of NO and pro-inflammatory mediators. Moreover, it downregulated iNOS in LPS-stimulated RAW264.7 cells, suppressed the release of pro-inflammatory cytokines, and decreased ROS levels in mice exposed to cigarette smoke (CS) and LPS. These results imply that AS has therapeutic and prophylactic potential in the airway inflammatory response associated with COPD.

Topics: Animals; Bronchoalveolar Lavage Fluid; Cell Death; Cell Survival; Cytokines; Disease Models, Animal; Enzyme Induction; Heme Oxygenase-1; Inflammation Mediators; Lipopolysaccharides; Lung; Macrophages; Male; Mice; Mice, Inbred C57BL; Neutrophils; Nitric Oxide; Nitric Oxide Synthase Type II; Pneumonia; RAW 264.7 Cells; Reactive Oxygen Species; RNA, Messenger; Smoking; Xanthophylls

2019