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• W3080857858 abstract "Purpose: Cigarette smoke (CS), a major causative agent of chronic obstructive pulmonary disease (COPD), induces lung cell death by incompletely understood mechanisms. The induction of apoptosis in lung structural cells by CS may contribute to the pathogenesis of emphysema. Phosphodiesterase-4 (PDE4) inhibitors are anti-inflammatory agents used in COPD therapy that can prevent CS-induced emphysema in mice. We investigated the effect of Rolipram, a first generation PDE4 inhibitor, on the regulation of CS-induced apoptosis. Methods: Human lung fibroblast (MRC-5) cells were exposed to cigarette smoke extract (CSE). Cell viability and apoptosis were determined by MTT assay and Annexin-V staining, respectively. Nuclear morphology was determined by Hoechst staining. Caspase activation was determined by Western analysis. Results: Rolipram protected against cell death and increased viability in MRC-5 fibroblasts after CSE exposure. Rolipram protected against apoptosis, decreased caspase-3 and -8 cleavage, and prevented nuclear condensation and fragmentation in MRC-5 cells exposed to CSE. Pretreatment with Rolipram enhanced Akt phosphorylation and associated cytoprotecion in CSE-treated cells, which could be reversed by the PI3K inhibitor LY294002. Conclusions: Rolipram protects against apoptosis of MRC-5 cells through inhibition of caspases-3 and -8. Rolipram may represent an effective therapeutic agent to reduce CS-induced apoptosis of lung fibroblasts." @default.
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• W3080857858 date "2012-01-01" @default.
• W3080857858 modified "2023-09-24" @default.
• W3080857858 title "Effect of Phosphodiestrase 4 inhibitor against Cigarette Smoke Extract Induced Autophagy and Apoptosis in Human Lung Fibroblasts (MRC-5 Cells)" @default.
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