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作 者:邱扬 陈龙飞 王晓玉[3] 林绍强[3] QIU Yang;CHEN Long-fei;WANG Xiao-yu;LIN Shao-qiang(Jiangmen Wuyi Hospital of Traditional Chinese Medicine,Jiangmen,Guangdong,China,529000;Foshan First People's Hospital,Foshan,Guangdong,China,528010;The First Affiliated Hospital of Jinan University,Guangzhou,Guangdong,China,510630)
机构地区:[1]江门市五邑中医院,广东江门529000 [2]佛山市第一人民医院,广东佛山528010 [3]暨南大学附属第一医院,广东广州510630
出 处:《河南中医》2021年第5期726-731,共6页Henan Traditional Chinese Medicine
摘 要:目的:研究姜黄素类似物L50H8对卵巢癌SKOV3细胞增殖和凋亡的影响,并探讨其作用机制。方法:用MTT法检测L50H8对细胞增殖的影响;Annexin V/PI双染色流式细胞法检测L50H8对细胞凋亡的影响;Western Blot法探讨L50H8诱导细胞凋亡的机制,检测其对Bax、凋亡诱导因子AIF、线粒体Caspase通路蛋白Caspase8、cleaved-caspase3、内质网应激启动因子GRP78及前凋亡因子CHOP表达的影响。结果:L50H8能显著抑制SKOV3细胞增殖,24 h的IC50低于其母体姜黄素的1/3。L50H8能诱导SKOV3细胞凋亡,其凋亡诱导效应强于姜黄素。Western Blot法发现L50H8能上调Bax与AIF表达,对Caspase8表达无明显影响,cleaved-caspase3未表达;L50H8能上调GRP78及CHOP的表达。结论:L50H8能显著抑制SKOV3细胞增殖、诱导细胞凋亡,其凋亡诱导效应可能通过上调Bax、激活AIF以及诱发内质网应激实现,但不依赖于线粒体Caspase通路。Objective:To research on the effect of curcumin analogue L50 H8 on proliferation and apoptosis of ovarian cancer SKOV3 cells and its mechanism.Methods:MTT was used to detect the effect of L50 H8 on cell proliferation.Annexin V/PI double staining flow cytometry was used to detect the effect of L50 H8 on apoptosis.Western Blot was used to investigate the mechanism of L50 H8 inducing apoptosis,and detect the effects of L50 H8 on Bax,AIF,caspase8,cleaved-caspase3,GRP78 and CHOP expression.Results:L50 H8 could significantly inhibit the proliferation of SKOV3 cells,the IC50 of 24 h was lower than 1/3 of curcumin.L50 H8 could induce apoptosis of SKOV3 cells,and its apoptosis inducing effect was stronger than that of curcumin.Western BLOT showed that L50 H8 could up-regulate the expressions of Bax and AIF,but had no significant effect on the expression of caspase8.Cleaved-caspase3 was not expressed.L50 H8 could up-regulate the expressions of GRP78 and CHOP.Conclusion:L50 H8 can significantly inhibit the proliferation of SKOV3 cells and induce apoptosis,which may be achieved by up-regulating Bax,activating AIF and inducing endoplasmic reticulum stress,but not by mitochondrial caspase pathway.
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