| In Vitro |
Milatuzumaba(5 μg/mL;8-48 小时)增强 MCL 细胞系和原发性患者肿瘤细胞的细胞死亡[1]。 Milatuzumaba(5 μg/mL;0.5-2 h)在 Jeko、Mino 和 SP-53 细胞中介导细胞毒性,部分取决于 ROS 的产生和线粒体跨膜电位的丧失[1]。 Milatuzumaba(5 μg/mL;4 小时)抑制 NF-κB 通路并诱导细胞凋亡,凋亡机制与 caspase 裂解、Bcl-2 家族成员失调或诱导自噬无关[1]。 Western Blot Analysis[1] Cell Line: Jeko and Mino cells Concentration: 5 μg/mL Incubation Time: 4 hours Result: Insignificant down-regulation of antiapoptotic proteins, such as Bax, Bcl-2, Bcl-xL, and Mcl-1. Cell Viability Assay[1] Cell Line: MCL cell lines and primarypatient tumor cells Concentration: 5 μg/mL Incubation Time: 8, 24, and 48 hours Result: Resulted in cell death of Jeko, Mino, SP-53, Rec-1, HBL-2, and Granta cells. Immunofluorescence[1] Cell Line: Jeko, Mino, and SP-53 cells Concentration: 5 μg/mL; with or without 10 mM N-acetylcysteine (HY-B0215) for 1.5 h Incubation Time: 0.5, 1, 1.5, and 2 hours Result: Increased ROS generation as early as 0.5 hours, while peaking at 1 to 1.5 hours and reducing at 2 hours.Therefore, it resulted cell death, but reserved by nonspecific ROS scavenger.
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