Liu Li-Bo, Xie Hui, Xue Yi-Xue, Liu Yun-Hui, Li Zhen, Wang Ping
Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang 110001, PR China; Institute of Pathology and Pathophysiology, China Medical University, Shenyang 110001, PR China.
Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang 110001, PR China; Institute of Pathology and Pathophysiology, China Medical University, Shenyang 110001, PR China.
Biochem Biophys Res Commun. 2015 Feb 20;457(4):595-601. doi: 10.1016/j.bbrc.2015.01.030. Epub 2015 Jan 16.
The present study was performed to examine whether Endothelial-monocyte-activating polypeptide II (EMAP II) could inhibit glioma growth by inducing rat brain glioma C6 cells apoptosis. The results revealed that the EMAP II decreased cell viability of rat C6 glioma cells in a time-dependent manner. Apoptotic proportion was increased gradually after EMAP II. EMAP II induced the decrease in mitochondrial membrane potential and the release of cytochrome c into the cytosol, followed by activation of caspase-9 and caspase-3. Meanwhile, EMAP II-induced apoptosis was accompanied by an increase of reactive oxygen species (ROS). The significant up-regulation in the expressions of Bax and Apaf-1 as well as down-regulation in the expression of Bcl-2 was observed. The time course change of ROS was prior to the changes of above investigated indexes. All of these results strongly suggest that EMAP II could induce rat C6 glioma cells apoptosis via the mitochondrial pathway, and ROS, Bax/Bcl-2 might be involved in this processing.
本研究旨在探讨内皮单核细胞激活多肽II（EMAP II）是否可通过诱导大鼠脑胶质瘤C6细胞凋亡来抑制胶质瘤生长。结果显示，EMAP II以时间依赖性方式降低大鼠C6胶质瘤细胞的活力。EMAP II作用后凋亡比例逐渐增加。EMAP II导致线粒体膜电位降低以及细胞色素c释放到细胞质中，随后激活半胱天冬酶-9和半胱天冬酶-3。同时，EMAP II诱导的凋亡伴随着活性氧（ROS）的增加。观察到Bax和Apaf-1表达显著上调以及Bcl-2表达下调。ROS的时间进程变化先于上述研究指标的变化。所有这些结果强烈表明，EMAP II可通过线粒体途径诱导大鼠C6胶质瘤细胞凋亡，且ROS、Bax/Bcl-2可能参与此过程。
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