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首页> 外文期刊>In vivo. >Lauryl Gallate Induces Apoptotic Cell Death through Caspase-dependent Pathway in U87 Human Glioblastoma Cells In Vitro
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Lauryl Gallate Induces Apoptotic Cell Death through Caspase-dependent Pathway in U87 Human Glioblastoma Cells In Vitro

机译:月桂基没食子酸酯通过U87人胶质母细胞瘤细胞中的胱天蛋白酶依赖性途径诱导凋亡细胞死亡。

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摘要

Background/Aim: The treatment of human glioma tumor is still an unmet medical need. Natural products are always promising resources for discovery of anticancer drugs. Lauryl gallate (LG) is one of the derivatives of gallic acid, widely present in plants, that has been shown to induce anticancer activities in many human cancer cell lines; however, it has not been studied in human glioma cell lines. Thus, the effects of LG on human glioblastoma U87 cells were investigated in the present in vitro study. Materials and Methods: Cell morphology and viability were examined by phase-contrast microscopy. Annexin V/Propidium iodide (PI) double staining were performed and assayed by flow cytometry to confirm that viable cell number reduction was due to the induction of apoptosis. Furthermore, U87 cells were exposed to LG in various concentrations and were analyzed by caspase activity assay. To further confirm that LG induced apoptotic cell death, the expression of apoptosis-associated proteins in LG-treated U87 cells was tested by western blot. Results: LG induced morphological changes and decreased viability in U87 cells. Annexin V/PI double staining revealed that LG induced apoptotic cell death in U87 cells in a dose-dependent manner. The increased activities of caspase-2, -3, -8 and -9 demonstrated that LG induced U87 cell apoptosis through a caspase-dependent pathway. In terms of molecular level, LG increased pro-apoptotic proteins Bax and Bak and decreased anti-apoptotic protein Bcl-2 in U87 cells. Furthermore, LG also suppressed the expression of p-Akt, Pak1, Hif-1 and Hif-2, {beta}-catenin and Tcf-1 in U87 cells. Conclusion: These results suggest that LG induced apoptotic cell death via the caspase-dependent pathway in U87 cells.
机译:背景/目的:人类神经胶质瘤肿瘤的治疗仍未满足医疗需求。天然产物一直是发现抗癌药物的有前途的资源。没食子酸月桂酸酯(LG)是广泛存在于植物中的没食子酸的衍生物之一,已证明在许多人类癌细胞系中会诱导抗癌活性;但是,尚未在人神经胶质瘤细胞系中进行研究。因此,在本体外研究中研究了LG对人胶质母细胞瘤U87细胞的作用。材料和方法:通过相差显微镜检查细胞形态和活力。进行膜联蛋白V /碘化丙啶(PI)双重染色,并通过流式细胞仪进行分析,以确认存活的细胞数量减少是由于凋亡的诱导。此外,将U87细胞以各种浓度暴露于LG,并通过胱天蛋白酶活性分析进行分析。为了进一步证实LG诱导凋亡的细胞死亡,通过Western印迹检测了LG处理的U87细胞中凋亡相关蛋白的表达。结果:LG诱导了U87细胞的形态变化和活力降低。 Annexin V / PI双重染色显示LG以剂量依赖性方式诱导U87细胞凋亡。 caspase-2,-3,-8和-9活性的增加表明LG通过caspase依赖性途径诱导U87细胞凋亡。在分子水平上,LG可增加U87细胞中的促凋亡蛋白Bax和Bak并降低抗凋亡蛋白Bcl-2。此外,LG还抑制了U87细胞中p-Akt,Pak1,Hif-1和Hif-2,β-catenin和Tcf-1的表达。结论:这些结果表明LG通过caspase依赖性途径诱导U87细胞凋亡。

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