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高压氧诱导的T淋巴细胞白血病和B淋巴细胞骨髓瘤癌细胞凋亡增加了p38丝裂原活化蛋白激酶的磷酸化。

Apoptosis of T-leukemia and B-myeloma cancer cells induced by hyperbaric oxygen increased phosphorylation of p38 MAPK.

作者信息

Chen Yen-Chen, Chen Shao-Yuan, Ho Pey-Shen, Lin Chia-Huei, Cheng Ya-Yuan, Wang Jehng-Kang, Sytwu Huey-Kang

机构信息

Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan, ROC.

出版信息

Leuk Res. 2007 Jun;31(6):805-15. doi: 10.1016/j.leukres.2006.09.016. Epub 2006 Oct 24.

DOI:10.1016/j.leukres.2006.09.016
PMID:17064767
Abstract

Tumor cells with different origins have different threshold to apoptosis. Hematopoietic (Jurkat, NCI-H929) cells and non-hematopoietic (A549, MCF-7) cells were received hyperbaric oxygen (HBO(2)) treatment from 2.5 to 3.5 atmosphere absolute (ATA) of 100% oxygen for 6h, and a significant percentage of apoptosis were shown only in hematopoietic Jurkat and NCI-H929 cells by either Annexin V or TUNEL assay. Oxidative stress was illustrated higher in HBO(2)-treated hematopoietic cells by superoxide fluorochrome detectors. HBO(2) treatment leads to caspase-3, caspase-7 activation and further cleavage of PARP within cells. Furthermore, the increased phosphorylation of p38 MAPK was demonstrated in both Jurkat and NCI-H929 cells.

摘要

不同起源的肿瘤细胞对细胞凋亡具有不同的阈值。造血细胞(Jurkat、NCI-H929)和非造血细胞(A549、MCF-7)接受了高压氧(HBO₂)处理,在100%氧气的2.5至3.5绝对大气压(ATA)下处理6小时,通过膜联蛋白V或TUNEL检测发现,只有造血的Jurkat和NCI-H929细胞出现了显著比例的凋亡。超氧化物荧光染料探测器显示,经HBO₂处理的造血细胞中的氧化应激更高。HBO₂处理导致细胞内半胱天冬酶-3、半胱天冬酶-7激活以及PARP的进一步裂解。此外,在Jurkat和NCI-H929细胞中均证实p38丝裂原活化蛋白激酶的磷酸化增加。

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