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海洋细菌 Cobetia marina 的荚膜多糖通过 caspase 依赖性和线粒体介导的途径诱导 HL-60 细胞凋亡。

Capsular polysaccharide from the marine bacterium Cobetia marina induces apoptosis via both caspase-dependent and mitochondria-mediated pathways in HL-60 cells.

机构信息

G.B. Elyakov Pacific Institute of Bioorganic Chemistry, Far Eastern Branch, Russian Academy of Sciences, 159/2, Prospect 100 let Vladivostoku, Vladivostok 690022, Russian Federation.

G.B. Elyakov Pacific Institute of Bioorganic Chemistry, Far Eastern Branch, Russian Academy of Sciences, 159/2, Prospect 100 let Vladivostoku, Vladivostok 690022, Russian Federation.

出版信息

Carbohydr Polym. 2025 Jan 1;347:122791. doi: 10.1016/j.carbpol.2024.122791. Epub 2024 Sep 22.

DOI:10.1016/j.carbpol.2024.122791
PMID:39487004
Abstract

In the present study, we investigated the antiproliferative effect of the capsular polysaccharide (CPS) from marine Gram-negative bacterium Cobetia marina (formerly C. pacifica) KMM 3878 against human leukemia cells in vitro and the potential molecular mechanism underlying this activity. Our results showed that the CPS could inhibit the proliferation of HL-60 cells in a dose-dependent manner with no effect on normal PBMC cells. HL-60 cells treated with the CPS exhibited typical morphologic and biochemical signs of apoptosis. We found that the CPS caused the collapse of mitochondrial transmembrane potential (ΔΨm), activated caspases-8,-9, and - 3, decreased the ratio of anti-apoptotic Bcl-2 and pro-apoptotic Bax proteins, increased ROS production and TNF-α secretion, and stimulated phosphorylation of p38 MAPK and p53 in HL-60 cells. Taken together, these data suggest that both extracellular and intracellular signaling pathways contribute to the CPS-induced apoptosis in HL-60 cells.

摘要

在本研究中,我们研究了海洋革兰氏阴性菌 Cobetia marina(原 C. pacifica)KMM 3878 的荚膜多糖(CPS)对体外人白血病细胞的抗增殖作用及其潜在的分子机制。我们的结果表明,CPS 可以剂量依赖性地抑制 HL-60 细胞的增殖,而对正常 PBMC 细胞没有影响。用 CPS 处理的 HL-60 细胞表现出典型的凋亡形态和生化特征。我们发现 CPS 导致线粒体跨膜电位(ΔΨm)崩溃,激活 caspase-8、-9 和 -3,降低抗凋亡 Bcl-2 和促凋亡 Bax 蛋白的比例,增加 ROS 产生和 TNF-α 分泌,并刺激 p38 MAPK 和 p53 在 HL-60 细胞中的磷酸化。综上所述,这些数据表明,细胞外和细胞内信号通路都参与了 CPS 诱导的 HL-60 细胞凋亡。

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