APO-9′-Fucoxanthinone Extracted from Undariopsis peteseniana Protects Oxidative Stress-Mediated Apoptosis in Cigarette Smoke-Exposed Human Airway Epithelial Cells

被引:13
作者
Jang, Jun-Ho [1 ,2 ]
Lee, Ji-Hyeok [3 ]
Chand, Hitendra S. [4 ]
Lee, Jong-Soo [5 ]
Lin, Yong [4 ]
Weathington, Nathaniel [1 ]
Mallampalli, Rama [1 ,2 ]
Jeon, You-Jin [3 ]
Nyunoya, Toru [1 ,2 ]
机构
[1] Univ Pittsburgh, Dept Med, Pittsburgh, PA 15213 USA
[2] VA Pittsburgh Healthcare Syst, Med Specialty Serv Line, Pittsburgh, PA 15240 USA
[3] Jeju Natl Univ, Dept Marine Sci, Jeju 690756, South Korea
[4] Lovelace Resp Res Inst, Albuquerque, NM 87108 USA
[5] Gyeongsang Natl Univ, Inst Marine Ind, Dept Seafood Sci & Technol, Tongyeong 650160, South Korea
关键词
brown algae; apo-9 '-fucoxanthinone; cigarette smoke; airway epithelial cells; DNA damage; apoptosis; oxidative stress; BROWN ALGA; DNA-DAMAGE; ECKLONIA-CAVA; CELLULAR SENESCENCE; CANCER CELLS; IN-VITRO; PHLOROTANNINS; LUNG; FUCOSTEROL; INHIBITION;
D O I
10.3390/md14070140
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Long-term cigarette smoking increases the risk for chronic obstructive pulmonary disease (COPD), characterized by irreversible expiratory airflow limitation. The pathogenesis of COPD involves oxidative stress and chronic inflammation. Various natural marine compounds possess both anti-oxidant and anti-inflammatory properties, but few have been tested for their efficacy in COPD models. In this study, we conducted an in vitro screening test to identify natural compounds isolated from various brown algae species that might provide protection against cigarette smoke extract (CSE)-induced cytotoxicity. Among nine selected natural compounds, apo-9'-fucoxanthinone (Apo9F) exhibited the highest protection against CSE-induced cytotoxicity in immortalized human bronchial epithelial cells (HBEC2). Furthermore, the protective effects of Apo9F were observed to be associated with a significant reduction in apoptotic cell death, DNA damage, and the levels of mitochondrial reactive oxygen species (ROS) released from CSE-exposed HBEC2 cells. These results suggest that Apo9F protects against CSE-induced DNA damage and apoptosis by regulating mitochondrial ROS production.
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页数:14
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