中文摘要：

Fucoidan 是从棕色的海草孤立的主要 sulfated 多糖之一。在这研究，我们在弥漫的大 B 房间淋巴瘤(DLBCL ) 上决定了 fucoidan 的反癌症活动在 vitro 并且在 vivo 的房间。Fucoidan 在一个剂量依赖者和时间依赖者举止禁止了 DLBCL 细胞的生长，并且 fucoidan 治疗挑起了 G ₀/G₁ 细胞周期拘捕，它被 p21 伴随起来规定和 cyclin D1， Cdk4，和 Cdk6 下面规定。Fucoidan 也在 DLBCL 房间线和主要 DLBCL 房间导致了 caspase 依赖的房间 apoptosis。另外， fucoidan 治疗从线粒体引起了 mitochondrial 膜潜力的损失和细胞色素 c 和导致 apoptosis 因素的版本进 cytosol。Fucoidan 也加强了在杀死 DLBCL 房间的 carfilzomib 的活动。fucoidan 的口头的管理有效地在异种皮移植老鼠模型禁止了肿瘤生长。我们的调查结果作为一个 anti-DLBCL 代理人揭示 fucoidan 的新奇功能，它能在 DLBCL 的临床的治疗被使用。

英文摘要：

Fucoidan is one of the major sulfated polysaccharides isolated from brown seaweeds. In this study, we determined the anti-cancer activity of fucoidan on diffuse large B cell lymphoma （DLBCL） cells both in vitro and in vivo. Fucoidan inhibited the growth of DLBCL cells in a dose- and time-dependent manner, and fucoidan treatment provoked G0/G1 cell cycle arrest, which was accompanied by p21 up-regulation and cyclin D1, Cdk4, and Cdk6 down-regulation. Fucoidan also induced caspase- dependent cell apoptosis in DLBCL cell lines and primary DLBCL cell. In addition, fucoidan treatment caused the loss of mitochondrial membrane potential and the release of cytochrome c and apop- tosis-inducing factor from the mitochondria into the cytosol. Fucoidan also potentiated the activities of carfilzomib in killing DLBCL cells. Oral administration of fucoidan effectively inhibited tumor growth in xenograft mouse models. Our findings reveal the novel function of fucoidan as an anti- DLBCL agent, which can be used in the clinical treatment of DLBCL.