摘要
目的 探讨细胞线粒体跨膜电位 (Δψm)和半胱氨酶3(Caspase 3)在三氧化二砷 (As2 O3 )诱导肿瘤细胞凋亡过程中的作用。方法 以Namalwa、SGC790 1和Bcap37细胞为体外模型 ,流式细胞仪检测亚G1期细胞含量和细胞膜磷脂酰丝氨酸 (PS)外翻量等方法鉴定细胞凋亡 ;碘化丙啶 (PI) /Rhodamine(Rh12 3)双染色检测Δψm变化并观察了Caspase 3抑制剂DEVD CHO对As2 O3 诱导肿瘤细胞凋亡的影响。结果 As2 O3 诱导肿瘤细胞凋亡效应与其诱导细胞Δψm下降和Caspase 3活性升高相关 ,抑制Caspase 3活性后As2 O3 使细胞选择坏死通路。结论 As2 O3 可能通过诱导细胞Δψm下降激活Caspase 3并最终使肿瘤细胞凋亡。
AIM To investigate the possible role of the mitochondrial transmembrane potential (Δψm) and caspase 3 in arsenic trioxide(As 2O 3)-induced apoptosis of cancer cells. METHOD Namalwa, SGC7901 and Bcap37 cell lines were used as in vitro models. Apoptosis was confirmed by sub-G 1 cells content as well as phosphatidylserine(PS) externalization. The Δψm was detected on flow cytometry through double staining of Rhodamine 123(Rh123) and popidium iodide(PI). In addition, the effect of DEVD-CHO, a selective inhibitor of Caspase 3, on As 2O 3-induced apoptosis was studied. RESULT The As 2O 3-induced apoptosis closely associated with the externalization of the Δψm and the activation of Caspase 3. As 2O 3 induced cells necrosis when Caspase 3 was inhibited. CONCLUSION As 2O 3 may selectively activates Caspase 3 after it induces externalization of Δψm, which causes cancer cells apoptosis.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2002年第1期87-90,共4页
Chinese Pharmacological Bulletin
