Article Sidebar
Published:
May 4, 2017DOI:
10.4314/tjpr.v16i4.7Keywords:
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
Sevoflurane anesthesia induces apoptosis and cell cycle arrest in NPC-039 nasopharyngeal cells
Abstract
Purpose: To determine the effects of sevoflurane on NPC-039 nasopharyngeal carcinoma cells.
Methods: WST-8 assays and flow cytometry with annexin V/PI staining were used to analyze the effects of sevoflurane on growth and induction of apoptotic changes in NPC-039 cells. Cell viability was performed on a microplate reader.
Results: Treatment of NPC-039 cells with 4 – 10 μM sevoflurane significantly inhibited cell growth (p < 0.005) with a median inhibitory concentration of 6 μM. NPC-039 cells incubated with sevoflurane showed prominent nuclear fragmentation and chromatin condensation. NPC-039 cells that exhibited apoptotic symptoms increased from 23.34 to 56.77 % when duration of treatment was increased from 24 to 48 h. Sevoflurane-treated cells also expressed increased levels of Bax and cleaved caspase-3. Reactive oxygen species formation was also higher in sevoflurane-treated NPC-039 cells than in control. Pre-treatment with Z-VAD-FMK followed by incubation with sevoflurane partly reduced the population of apoptotic NPC-039 cells compared with cells treated with sevoflurane alone. The proportion of cells in S- and G0/G1 phases decreased and increased, respectively, when sevoflurane concentration was increased from 2 to 10 μM. Incubating NPC-039 cells with sevoflurane also markedly reduced levels of cyclin-dependent kinases including p15 INK4B, cyclin D1, p16 INK4A, and CDK-6. In contrast, pretreatment with ZVAD-FMK followed by incubation with sevoflurane increased p15 INK4B levels.
Conclusion: Sevoflurane inhibits nasopharyngeal carcinoma cell growth, activating apoptosis and inducing cell cycle arrest, thus suggesting its therapeutic potential for the treatment of nasopharyngeal carcinoma.
Keywords: Sevoflurane, Nasopharyngeal carcinoma, Chromatin, Condensation
