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首页> 外文期刊>Pharmacognosy magazine >Luffa echinata Roxb. Induced Apoptosis in Human Colon Cancer Cell (SW-480) in the Caspase-dependent Manner and Through a Mitochondrial Apoptosis Pathway
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Luffa echinata Roxb. Induced Apoptosis in Human Colon Cancer Cell (SW-480) in the Caspase-dependent Manner and Through a Mitochondrial Apoptosis Pathway

机译:丝瓜紫锥菊Roxb。通过半胱天冬酶依赖性方式并通过线粒体凋亡途径诱导人结肠癌细胞(SW-480)凋亡

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摘要

Background: Luffa echinata Roxb. (LER) (Cucurbitaceae) showed tremendous medicinal importance and are being used for the treatment of different ailments. Objective: In this study, the antiproliferative properties and cell death mechanism induced by the extract of the fruits of LER were investigated. Materials and Methods: MTT and LDH assay were used to test the antiproliferative and cytotoxicity of LER extract, respectively. The intracellular ROS were measured by a fluorometric assay. The expression of several apoptotic-related proteins in SW-480 cells treated by LER was evaluated by Western blot analysis. Results: The methanolic extract of LER fruits inhibited the proliferation of human colon cancer cells (SW-480) in both dose- and time-dependent manners. The LER-treated cells showed obvious characteristics of cell apoptosis, including cell shrinkage, destruction of the monolayer, and condensed chromatin. In addition, treatments of various concentrations of LER extracts caused the release of lactate dehydrogenase as a dose-dependent manner via stimulation of the intracellular metabolic system. LER induced apoptosis, DNA fragmentation, and cellular ROS accumulation in SW-480 cells. Treatment of LER on SW-480 cells promoted the expression of caspases, Bax, Bad, and p53 proteins and decreased the levels of Bcl-2 and Bcl-XL. Conclusions: These results indicated that treatment with LER-induced cell death in mitochondrial apoptosis pathway by regulating pro-apoptotic proteins via the up regulation of the p53 protein. These findings highlight the potentials of LER in the treatment of human colon cancer. SUMMARY LER induced apoptosis, DNA fragmentation, and cellular ROS accumulation in SW-480 cells. Treatment of LER on SW-480 cells promoted the expression of caspases, Bax, Bad, and p53 proteins and decreased the levels of Bcl-2 and Bcl-XL.
机译:背景:丝瓜紫锥菊Roxb。 (LER)(葫芦科)具有极大的医学重要性,正在被用于治疗各种疾病。目的:研究LER提取物诱导的抗增殖特性和细胞死亡机制。材料与方法:MTT法和LDH法分别检测LER提取物的抗增殖和细胞毒性。通过荧光测定法测量细胞内ROS。通过蛋白质印迹分析评估了LER处理的SW-480细胞中几种凋亡相关蛋白的表达。结果:LER果实的甲醇提取物以剂量和时间依赖性方式抑制人结肠癌细胞(SW-480)的增殖。 LER处理的细胞显示出明显的细胞凋亡特征,包括细胞萎缩,单层破坏和染色质浓缩。另外,各种浓度的LER提取物的处理通过刺激细胞内代谢系统以剂量依赖性方式引起乳酸脱氢酶的释放。 LER诱导SW-480细胞凋亡,DNA片段化和细胞ROS积累。 LER在SW-480细胞上的处理促进了胱天蛋白酶,Bax,Bad和p53蛋白的表达,并降低了Bcl-2和Bcl-XL的水平。结论:这些结果表明,通过上调p53蛋白来调节促凋亡蛋白,以LER诱导的线粒体凋亡途径中的细胞死亡。这些发现突出了LER在治疗人类结肠癌中的潜力。小结LER诱导SW-480细胞凋亡,DNA片段化和细胞ROS积累。 LER在SW-480细胞上的处理促进了胱天蛋白酶,Bax,Bad和p53蛋白的表达,并降低了Bcl-2和Bcl-XL的水平。

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