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Bax/Bcl-2 比值的改变促成了诃子诱导的人肺癌和乳腺癌细胞凋亡。

Alteration of Bax/Bcl-2 ratio contributes to Terminalia belerica-induced apoptosis in human lung and breast carcinoma.

作者信息

Ghate Nikhil Baban, Hazra Bibhabasu, Sarkar Rhitajit, Chaudhuri Dipankar, Mandal Nripendranath

机构信息

Division of Molecular Medicine, Bose Institute, P-1/12 C. I. T. Scheme VII M, Kolkata, 700054, India.

出版信息

In Vitro Cell Dev Biol Anim. 2014 Jun;50(6):527-37. doi: 10.1007/s11626-013-9726-x. Epub 2014 Jan 8.

Abstract

The objective of the present study was to assess the in vitro anticancer activity of 70% methanolic extract of Terminalia belerica (TBME) against human lung (A549) and human breast (MCF-7) carcinoma and its possible mechanism. TBME showed significant cytotoxicity to both A549 and MCF-7 cells, whereas, no cytotoxicity was found in non-malignant WI-38 cells. Flow cytometric analysis was then performed and 100 μg/ml of TBME was selected as the effective concentration inducing apoptosis in A549 and MCF-7. At this concentration, TBME caused DNA fragmentation pattern of apoptosis. Furthermore, mechanism of apoptosis induction was demonstrated using western blotting and Bax/Bcl-2 ratio in both types of the cells was found increased, which leads to the activation of caspase cascade along with the cleavage of PARP. These results suggested that TBME is able to induce anticancer effects on both lung and breast cancer cell lines through the modulation of Bcl-2 family proteins.

摘要

本研究的目的是评估诃子70%甲醇提取物(TBME)对人肺癌(A549)和人乳腺癌(MCF-7)细胞的体外抗癌活性及其可能的作用机制。TBME对A549和MCF-7细胞均表现出显著的细胞毒性,而在非恶性的WI-38细胞中未发现细胞毒性。随后进行了流式细胞术分析,并选择100μg/ml的TBME作为诱导A549和MCF-7细胞凋亡的有效浓度。在此浓度下,TBME导致了凋亡的DNA片段化模式。此外,通过蛋白质印迹法证实了凋亡诱导机制,并且发现两种细胞中的Bax/Bcl-2比值均升高,这导致了半胱天冬酶级联反应的激活以及PARP的裂解。这些结果表明,TBME能够通过调节Bcl-2家族蛋白对肺癌和乳腺癌细胞系产生抗癌作用。

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