1. Coniferyl aldehyde alleviates LPS-induced WI-38 cell apoptosis and inflammation injury via JAK2–STAT1 pathway in acute pneumonia
- Author
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Flávio Sano, Emanuel Sarinho, Antonio Carlos Pastorino, Dirceu Solé, Felipe Faria Pierotti, Magnus P. Borres, Renata Rodrigues Cocco, Herberto José Chong Neto, Jackeline Motta Franco, Maria Letícia Chavarria, Arnaldo Porto Neto, Neusa Falbo Wandalsen, Carolina Sanchez Aranda, Ana Carolina Rozalem Reali, Lilian Moraes, Nelson Rosario, and Ekaterini Goudouris
- Subjects
Pulmonary and Respiratory Medicine ,Intoxicative inhalant ,medicine.medical_specialty ,education.field_of_study ,Allergy ,biology ,business.industry ,Immunology ,Population ,General Medicine ,Immunoglobulin E ,medicine.disease ,Dermatology ,Allergic sensitization ,biology.protein ,Immunology and Allergy ,Medicine ,Laboratory screening ,Food allergens ,business ,education ,Kappa - Abstract
Pneumonia is a kind of inflammatory disease characterized by pathogen infection of lower respiratory track. Lipopolysaccharide (LPS) is the main bioactive component of Gram-negative bacteria responsible for inflammatory response. Recently, coniferyl aldehyde (CA) has been reported to play a crucial role because of its anti-inflammatory activity. However, the effect and mechanisms of CA in ameliorating symptoms of acute pneumonia remain unknown. Evaluating and identifying the value and exploring the mechanisms of CA on LPS-mediated WI-38 apoptosis and inflammation were the aims of this study. Here, CCK-8 cell viability assay was applied on WI-38 after treatment with or without LPS at different doses of CA to verify that CA can increase LPS-induced cell viability. Then, quantitative polymerase chain reaction (qPCR) and enzyme-linked-immunosorbent serologic assays (ELISA) suggested that LPS treatment dramatically decreased the expression level of IL-10 (anti-inflammatory factor) while strikingly increasing the expression levels of IL-1β, IL-6, and TNF-α (tumor necrosis factor-α; proinflammatory factor) whereas CA treatment attenuates LPS-induced inflammation of WI-38. Further, flow cytometry and Western blot assay verified that LPS treatment dramatically promoted apoptosis of WI-38 cells, while administration of CA notably inhibited apoptosis of WI-38 cells. Moreover, the Western blot assay hinted that CA could inactivate LPS-induced JAK2–STAT1 signaling pathway. These findings indicated that CA could alleviate LPS-mediated WI-38 apoptosis and inflammation injury through JAK2–STAT1 pathway in acute pneumonia.
- Published
- 2021