Protein-Bound Polysaccharide K Partially Prevents Apoptosis of Circulating T Cells Induced by Anti-Cancer Drug S-1 in Patients with Gastric Cancer
Protein-Bound Polysaccharide K Partially Prevents Apoptosis of Circulating T Cells Induced by Anti-Cancer Drug S-1 in Patients with Gastric Cancer
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DOI：
10.1159/000151361
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发表时间：
2008-08
期刊：
影响因子：
3.5
通讯作者：
K. Kono;Y. Kawaguchi;Y. Mizukami;K. Mimura;H. Sugai;H. Akaike;H. Fujii
中科院分区：
文献类型：
--
作者：
K. Kono;Y. Kawaguchi;Y. Mizukami;K. Mimura;H. Sugai;H. Akaike;H. Fujii
背景和方法：研究表明，T细胞功能障碍，包括外周血T细胞凋亡，常见于接受化疗的患者中。为了评估同时服用口服生物反应调节剂蛋白结合多糖 K (PSK) 是否可以在接受抗癌药物 S-1 治疗的患者中诱导抗凋亡作用，分析了治愈性切除的 III 期胃癌患者的外周血 T 细胞的凋亡诱导、Caspase-3 活性以及促凋亡蛋白 Bax 和抗凋亡蛋白 Bcl-2 的表达，这些患者被随机分配到术后单独接受 S-1 辅助治疗（n = 10) 或 S-1 与 PSK 结合 (n = 10)。结果：辅助治疗后 5 周，S-1 组 (24.1 ± 5.0%) 的 T 细胞凋亡显着高于 S-1 + PSK 组 (19.1 ± 3.9%)。 S-1 诱导 T 细胞凋亡，同时升高外周血 T 细胞中的 caspase-3 活性和 Bax 表达。此外，PSK 部分阻止了 S-1 诱导的 T 细胞凋亡。结论：PSK可以部分阻止S-1诱导的T细胞凋亡。
Background and Methods:It has been shown that T-cell dysfunction, including apoptosis of peripheral blood T cells, commonly occurs in patients receiving chemotherapy. In order to evaluate whether concomitant administration of the oral biological response modifier protein-bound polysaccharide K (PSK) could induce anti-apoptotic effects in patients treated with the anti-cancer drug, S-1, peripheral blood T cells were analyzed for induction of apoptosis, caspase-3 activities and expression of proapoptotic protein Bax and anti-apoptotic protein Bcl-2 in patients with curatively resected stage III gastric cancer, who were randomly assigned to postoperative adjuvant therapy with S-1 alone (n = 10) or S-1 combined with PSK (n = 10). Results: T-cell apoptosis 5 weeks after adjuvant therapy was significantly higher in the S-1 group (24.1 ± 5.0%) than in the S-1 + PSK group (19.1 ± 3.9%). S-1 induced T-cell apoptosis and concomitantly elevated caspase-3 activities and Bax expression in peripheral blood T cells. In addition, PSK partially prevented the T-cell apoptosis induced by S-1. Conclusion:PSK could partially prevent the T-cell apoptosis induced by S-1.