[abstract] THE MECHANISM OF HYPERBARIC OXYGEN INDUCED APOPTOSIS OF B LYMPHOCYTE MYELOMA CELL LINE

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[abstract] THE MECHANISM OF HYPERBARIC OXYGEN INDUCED APOPTOSIS OF B LYMPHOCYTE MYELOMA CELL LINE

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Title: [abstract] THE MECHANISM OF HYPERBARIC OXYGEN INDUCED APOPTOSIS OF B LYMPHOCYTE MYELOMA CELL LINE
Author: Chen, SY; Lin, GH; Chen, YC; Cheng, YY; Chen, YJ
Abstract: BACKGROUND: Our previous finding showed that early HBO2 therapy exposure attenuated the severity of disease progression in NZB/W F1 mice. Although the mechanism remained unclear, our study suggested that HBO2-mediated immunosuppression targeted a particular cell population, specifically autoreactive lymphocytes. In addition, our another experiment was to treat Jurkat cell line at 3.6 ATA HBO2, 3.6 ATA HBA and incubator respectively for 6 hours. The results demonstrated significant apoptosis in HBO2 group by increased oxidative stress. After HBO2 treatment, the phosphorylation of p38 MAPK was increased and phosphorylation of ERK1/2 was decreased. Furthermore, caspase-3 and caspase-7 were activated and leading to the cleavage of PARP and apoptosis. In order to explore the possible mechanism of HBO2-induced apoptosis, the study is to investigate the different mechanism between Jurkat and NCI-H929 cell line. MATERIALS AND METHODS: The NCI-H929 cell line was exposed to 3.6 ATA HBO, 3.6 ATA HBA and incubator for 6 hours, respectively. The percentage of apoptotic cells was detected by AnnexinV/propidium iodide and Hoechst staining. The alteration in mitochondria membrane potential after HBO2 treatment was detected by DiOC6(3) fluorescence staining. Fas (CD-95) expression was tested by FITC-conjugated anti-Fas antibody and further analyzed by flow cytometry. The signaling pathway of HBO2-induced apoptosis in NCI-H929 cells were checked by western blotting including Mitogen-activated protein kinase (MAPK): p38, JNK and ERK1/2; p53, caspases including caspase-3, caspase-7 and PARP. RESULTS: The results demonstrated significant apoptosis and oxidative stress in HBO2 group. After HBO2 treatment, phosphorylation of p38 MAPK was increased and caspase-3, 7 were activated, then leading to the cleavage of PARP. Meanwhile, the phosphorylation of p53 was increased. CONCLUSIONS: Our results showed that HBO2 treatment increased intracellular oxidative stress in Jurkat and NCI-H929 cells, further leading to apoptosis. Furthermore, p53 might be involved in HBO2-induced apoptosis of NCI-H929 cell line.
Description: Undersea and Hyperbaric Medical Society, Inc. (http://www.uhms.org )
URI: http://archive.rubicon-foundation.org/1659
Date: 2005

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  • UHMS Meeting Abstracts
    This is a collection of the published abstracts from the Undersea and Hyperbaric Medical Society (UHMS) annual meetings.

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