OBJECTIVE: To investigate the effect of curcumin against cigarette smoke extract (CSE)- induced oxidative stress in human bronchial epithelial cells and explore the underlying mechanism. METHODS: Human bronchial epithelial cell line 16HBE was treated for 24 h with curcumin, CSE, CSE + curcumin, and CSE + curcumin with transfection by a short hairpin RNA targeting PPARγ (shPPARγ). MTT assay was used to observe the changes in the cell viability after the treatments. Quantitative real-time PCR was performed to detect the mRNA expressions of tumor necrosis factor-α (TNF-α), iNOS and PPARγ in the cells, and the protein expressions of iNOS, PPARγ and the phosphorylation of NF-κB p65 were detected using Western blotting. RESULTS: The treatments did not cause significant changes in the cell viability. Exposure to CSE for 24 h significantly lowered PPARγ expression and increased TNF-α and iNOS expressions and phosphorylation of NF-κB p65 in the cells. The effects of CSE were significantly suppressed by curcumin, but transfection of the cells with shRNA-PPARγ obviously abrogated the suppressive effects of curcumin. CONCLUSIONS: Curcumin suppresses CSE-induced oxidative stress and inflammation via the PPARγ/NF-κB signaling pathway in 16HBE cells, suggesting the potential of curcumin in the treatment of chronic obstructive pulmonary disease.
OBJECTIVE: To investigate the effect of curcumin against cigarette smoke extract (CSE)- induced oxidative stress in human bronchial epithelial cells and explore the underlying mechanism. METHODS:Human bronchial epithelial cell line 16HBE was treated for 24 h with curcumin, CSE, CSE + curcumin, and CSE + curcumin with transfection by a short hairpin RNA targeting PPARγ (shPPARγ). MTT assay was used to observe the changes in the cell viability after the treatments. Quantitative real-time PCR was performed to detect the mRNA expressions of tumor necrosis factor-α (TNF-α), iNOS and PPARγ in the cells, and the protein expressions of iNOS, PPARγ and the phosphorylation of NF-κB p65 were detected using Western blotting. RESULTS: The treatments did not cause significant changes in the cell viability. Exposure to CSE for 24 h significantly lowered PPARγ expression and increased TNF-α and iNOS expressions and phosphorylation of NF-κB p65 in the cells. The effects of CSE were significantly suppressed by curcumin, but transfection of the cells with shRNA-PPARγ obviously abrogated the suppressive effects of curcumin. CONCLUSIONS:Curcumin suppresses CSE-induced oxidative stress and inflammation via the PPARγ/NF-κB signaling pathway in 16HBE cells, suggesting the potential of curcumin in the treatment of chronic obstructive pulmonary disease.
Authors: Michael Seimetz; Nirmal Parajuli; Alexandra Pichl; Florian Veit; Grazyna Kwapiszewska; Friederike C Weisel; Katrin Milger; Bakytbek Egemnazarov; Agnieszka Turowska; Beate Fuchs; Sandeep Nikam; Markus Roth; Akylbek Sydykov; Thomas Medebach; Walter Klepetko; Peter Jaksch; Rio Dumitrascu; Holger Garn; Robert Voswinckel; Sawa Kostin; Werner Seeger; Ralph T Schermuly; Friedrich Grimminger; Hossein A Ghofrani; Norbert Weissmann Journal: Cell Date: 2011-10-14 Impact factor: 41.582
Authors: Teal S Hallstrand; Tillie L Hackett; William A Altemeier; Gustavo Matute-Bello; Philip M Hansbro; Darryl A Knight Journal: Clin Immunol Date: 2013-12-14 Impact factor: 3.969