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作 者:章平[1] 孙斌[1] 杨煌建[1] 庄秀园[1] 柏忠江[1] 王露[1] 瞿伟菁[1]
出 处:《华东师范大学学报(自然科学版)》2004年第4期91-96,共6页Journal of East China Normal University(Natural Science)
基 金:上海市科技发展基金项目(014358009)
摘 要:探讨了沙棘籽渣黄酮类化合物(flavonoids from seed residues of Hippophae rhamnoidesm L.FHR)对人乳腺癌Bcap-37细胞凋亡的影响和其作用机制.采用MTT法、Wright染色法、流式细胞术及免疫细胞化学等方法,观察在不同浓度和作用时间时,FHR对Bcap-37细胞生长抑制和细胞凋亡效应.结果显示FHR在10~1000μg/mL等浓度范围内可以诱导人乳腺癌细胞Bcap-37产生典型的凋亡形态学变化;1000μg/mL FHR处理24 h、48 h和72 h后使Bcap-37细胞周期S期减少,G0/G1期增加;FHR处理实验组p53蛋白表达较对照组明显增加,bcl-2蛋白表达较对照组降低.提示FHR对人乳腺癌Bcap-37细胞的生长抑制主要通过诱导细胞凋亡,且p53蛋白的增加和bcl-2蛋白的减少是其诱导细胞凋亡的机制之一.To investigate the effect and mechanism of apoptosis of human mammary carcinoma Bcap-37 cells induced by flavonoids from seed residues of Hippophae rhamnoides L. (FHR). Bcap-37 cells were treated by different concentration of FHR at diverse time periods, which was identified by MTT, Wright staining, flow cytometry and immunohistochemical methods. The experiments showed that FHR can induce Bcap-37 cells undergoing apoptosis within 10-1000 μg/mL, its apoptotic symptom depends on dose (FHR) and time gradient; the cell cycle of Bcap-37 cells was affected when it was treated 24 h, 28 h and 72 h with 1000 μg/mL FHRi S phase reduced, and G0/G1 increased; compared with the control group, the expression of p53 protein increased and bcl-2 protein decreased in Bcap-37 cells treated with FHR. These results suggest that FHR can trigger growth inhibition on Bcap-37 cells in vitro by inducing apoptosis, meanwhile the increase of p53 protein and decrease of bcl-2 protein is one of the reasons on mechanism of apoptosis.
关 键 词:沙棘 黄酮类化合物 人乳腺癌Bcap-37细胞 细胞凋亡
分 类 号:R255[医药卫生—中医内科学]
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