Resveratrol reduces the apoptosis induced by cigarette smoke extract by upregulating MFN2.
basic_science · Level V
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- Record sourced from PubMed, PMID 28406974.
- Also identified by DOI 10.1371/journal.pone.0175009 and PMC identifier 5391199.
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Abstract
The aim of this study was to investigate the effect of resveratrol (RSV) on cigarette smoke extract (CSE)-induced cell apoptosis and mitochondrial dysfunction in vitro, as well as changes in the MFN2 expression level. Cultured human bronchial epithelial (HBE) cells were initially treated with CSE to induce apoptosis, followed by incubation either with or without RSV. Numerous techniques were used to evaluate the outcomes of the present study, including a cell counting kit-8 assay, real-time quantitative polymerase chain reaction (real-time qPCR), western blotting, JC-1 fluorescence, Hoechst 33342 staining, Annexin V-PI flow cytometry apoptosis analyses, and siRNA technology. A 24 h incubation in 3.5% CSE induced apoptosis in HBE cells, and pretreatment of HBE cells with RSV (20 μM) significantly suppressed the CSE-induced apoptosis, prevented the CSE-induced decrease in MFN2 levels, suppressed BAX translocation to the mitochondria, and prevented mitochondrial membrane potential loss and cytochrome C release. However, following the transfection of MFN2 siRNA, the anti-apoptotic effects of RSV were significantly attenuated. The results of the present study demonstrated that RSV may protect bronchial epithelial cells from CS-induced apoptosis in vitro by preventing mitochondrial dysfunction, and MFN2 may be associated with the anti-apoptotic functions of RSV in HBE cells.
Medical subject headings
- Apoptosis
- Bronchi
- Complex Mixtures
- Epithelial Cells
- GTP Phosphohydrolases
- Mitochondrial Proteins
- Respiratory Mucosa
- Stilbenes
- Tobacco Smoke Pollution
- Up-Regulation