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机构地区:[1]中山大学病理生理学教研室,广东广州510080 [2]中山大学附属第三医院传染病科,广东广州510630
出 处:《中国病理生理杂志》2005年第10期1888-1891,共4页Chinese Journal of Pathophysiology
基 金:广东省重大科技专项基金资助项目(No.2004A30801006);国际合作项目(2004B50301003)
摘 要:目的:观察manumycin对人胰腺导管癌细胞Panc-1的抑制效应,并探讨其诱导细胞凋亡是否经 p38MAPK介导。方法:用MTT法检测manumycin对Panc-1细胞的抑癌作用。用caspase-3活性检测试剂盒定量检测 manumycin诱导细胞凋亡的水平及评估特异性的p38MAPK抑制剂SB203580对它的影响。结果:经manumycin (6/μmol/L、18/μmol/L、54 μmol/L)处理Panc-1细胞24 h,对Panc-1细胞生长具有明显的抑制作用,其抑制率分别为 8.9%、21.9%和67.0%,其中后二者的细胞活性与对照组相比有显著差异(P<0.01),呈量效关系。用药24 h的IC50 为34.7μmol/L。同时,此药物可明显增加caspase-3的活性,且这一效应可部分地被p38抑制剂SB203580阻断。结 论:Manumycin可通过诱导Panc-1细胞凋亡而产生抑癌作用,p38MAPK是manumycin诱导细胞凋亡的通路之一。AIM: In this study, we investigated the anticancer effect and mechanisms of manumycin on pancreatic cancer cell line -Panc - 1 and the role of p38MAPK pathway in apoptosis. METHODS: The test of anticancer effect was performed by MTT assay. Apoptosis was induced in the cells by manumycin and then treated with SB203580, a specific p38MAPK inhibitor. A quantitative caspase - 3 activity assay kit was used in this experiment. RESULTS: Manumyein (6μmol/L, 18μmol/L, 54μmol/ L) significantly inhibited cell growth of pancreatic cancer cell line Panc - 1. The inhibition rates 24 h after treatment with 6 μmol/ L, 18 μmol/L and 54 μmol/L manumycin were 8.9%, 21.9% and 67.0%, respectively. Compared with the control group, the survival levels of the last two groups were of significant statistical difference ( P 〈 0.01 ). The anticancer effects also showed dosage - effect relationship, the v.,due of IC50 24 h after treatment was 34.7 μmol/L. In addition, this reagent simultaneously activated caspase - 3 protein, which was partly blocked by p38MAPK specific inhibitor, SB203580. CONCLUSION: Manumycin exerted anticancer effect on Pane - 1 cell line via inducing cell apoptosis, which was partly regulated by p38MAPK.
关 键 词:MANUMYCIN 胰腺导管癌 细胞凋亡 P38MAP激酶
分 类 号:R735.905.3[医药卫生—肿瘤]
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