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首页> 外文期刊>Oncology letters >Evodiamine inhibits proliferation and induces apoptosis in gastric cancer cells
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Evodiamine inhibits proliferation and induces apoptosis in gastric cancer cells

机译:Evodiamine抑制胃癌细胞增殖并诱导其凋亡

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In the present study, the effects of evodiamine on the apoptosis of human gastric cancer cells was studied in order to assess its antitumor effects and identify the molecular mechanisms involved. SGC7901 gastric cancer cells were treated with evodiamine at various concentrations (0, 3, 6, 12, 24 and 48 mu mol/l) for 24 h. Inhibition of the proliferation of SGC7901 cells was assessed using an MTT assay. The morphology of treated SGC7901 cells was observed using optical microscopy; in addition, the effect of evodiamine on the nuclear morphology of cells was analyzed using Hoechst 33258 staining with fluorescence microscopy. Annexin V-fluorescein isothiocyanate/propidium iodide staining and flow cytometric analysis were used for investigating the effect of evodiamine on the induction of apoptosis in SGC7901 cells. Expression levels of survivin and caspase-3 were examined using reverse transcription polymerase chain reaction. The results demonstrated that evodiamine significantly inhibited SGC7901 cell proliferation (P<0.05) and induced apoptosis in a dose-dependent manner (P<0.05). Morphological characteristics of apoptosis were confirmed using optical microscopy and Hoechst 33258 staining analysis indicated that evodiamine treatment resulted in the typical characteristics of apoptotic programmed cell death, including cell shrinkage and apoptotic body formation. Flow cytometric analysis demonstrated that evodiamine induced the dose-dependent apoptosis of SGC7901 cells. Messenger (m)RNA levels of survivin decreased and those of caspase-3 increase in a dose-dependent manner in SGC7901 cells treated with various concentrations of evodiamine for 24 h. In conclusion, the results of the present study demonstrated that evodiamine inhibited proliferation and induced apoptosis in gastric cancer cells via the downregulation of survivin and upregulation of caspase-3 mRNA.
机译:在本研究中,研究了依维他命对人胃癌细胞凋亡的影响,以评估其抗肿瘤作用并确定涉及的分子机制。 SGC7901胃癌细胞用不同浓度(0、3、6、12、24和48μmol / l)的evodiamine处理24 h。使用MTT测定法评估SGC7901细胞的增殖抑制。用光学显微镜观察处理过的SGC7901细胞的形态。此外,使用Hoechst 33258染色和荧光显微镜分析了依维他命对细胞核形态的影响。 Annexin V-异硫氰酸荧光素/碘化丙啶染色和流式细胞仪分析用于研究依维他命对SGC7901细胞凋亡的诱导作用。使用逆转录聚合酶链反应检测survivin和caspase-3的表达水平。结果表明,依地洛明显着抑制SGC7901细胞增殖(P <0.05),并以剂量​​依赖性方式诱导细胞凋亡(P <0.05)。使用光学显微镜确认了凋亡的形态学特征,并且Hoechst 33258染色分析表明,依维多明治疗导致凋亡的程序性细胞死亡的典型特征,包括细胞收缩和凋亡小体形成。流式细胞仪分析表明,依维他命诱导了SGC7901细胞的剂量依赖性凋亡。在用不同浓度的依地洛明处理24 h的SGC7901细胞中,survivin的Messenger(m)RNA水平下降,而caspase-3的mRNA水平呈剂量依赖性。总之,本研究的结果表明,依维多胺通过下调survivin和上调caspase-3 mRNA抑制胃癌细胞的增殖并诱导其凋亡。

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