Affiliation:
1. Department of Respiratory and Critical Care Medicine, Shenzhen Longhua District Central Hospital, Shenzhen City 518110, Guangdong Province, China
Abstract
Cigarette smoke (CS) is a risk factor for chronic obstructive pulmonary disease (COPD), which can exacerbate inflammation and oxidative stress. Pristimerin (Pris) is a natural compound with antioxidant and anti-inflammatory effects. We managed to evaluate the protective effects of Pris on CS-induced COPD. The CS-induced COPD mice model and cell model were constructed. The effects of Pris treatment on lung function, inflammatory cell infiltration, myeloperoxidase (MPO), and pathological changes of lung tissues in mice model were evaluated. The impacts of Pris treatment on inflammatory factors, chemokines, and oxidative stress parameters in mice lung tissues and cells were determined by kits. The viability of human bronchial epithelial cells after Pris treatment was tested by CCK-8. The activation of NF-κB pathway was confirmed by Western blot and immunofluorescence. CS treatment impaired lung function, reduced weight of mice, and enhanced inflammatory cell infiltration, MPO, and lung tissue damage, but these effects of CS were reversed by Pris treatment. Furthermore, Pris treatment downregulated the levels of malondialdehyde, IL-6, IL-1β, TNF-α, CXCL1, and CXLC2, but upregulated superoxide dismutase and catalase levels. Pris treatment could overturn CS-induced activation of the NF-κB pathway. Pris alleviates CS-induced COPD by inactivating NF-κB pathway.
Funder
Shenzhen Foundation of Science and Technology
Guangdong Provincial Key Laboratory Disease Research
Publisher
Canadian Science Publishing
Subject
Cell Biology,Molecular Biology,Biochemistry
Cited by
8 articles.
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