3- o-乙酰-11-酮-β-乳香酸对MCF-7细胞的体外抗增殖和细胞周期阻滞电位。

IF 3.6 Q2 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Journal, genetic engineering & biotechnology Pub Date : 2023-07-02 DOI:10.1186/s43141-023-00529-2
Saja A Ahmed, Ahmed F Al-Shanon, Ali Z Al-Saffar, Alene Tawang, Jameel R Al-Obaidi
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摘要

导读:癌症是医学科学中的一个主要问题,全世界每年的死亡病例都在增加。因此,寻找高效、选择性和低毒性的替代疗法和非正统疗法是对抗癌症的主要目标。乙酰-11-酮-β-乳香酸(AKBA)是一种衍生的五环三萜化合物,具有多种生物活性,具有潜在的抗肿瘤作用。本研究利用AKBA在体外检测其对MCF-7细胞的潜在细胞毒活性,并监测其细胞和形态变化,以期对诱导凋亡产生预期影响。方法:采用3(4,5二甲基噻唑-2 -基)-2,5二苯四溴唑(MTT)法测定AKBA的细胞毒活性。检测到MCF-7细胞活力的剂量依赖性抑制。与未处理的MCF-7细胞相比,AKBA的增加显著抑制了MCF-7细胞的克隆原性。结果:在形态学上,MCF-7细胞暴露于高AKBA浓度下,细胞核形态发生改变,表现为细胞核大小和细胞通透性强度增加。随着AKBA浓度的增加,线粒体膜电位(ΔΨm)降低,细胞色素c显著释放。吖啶橙/溴化乙啶双染色实验证实,AKBA (IC50浓度)处理的MCF-7细胞表现为晚期凋亡,呈强烈而明亮的红色。结论:观察到活性氧形成显著增加。估计了Caspase 8和Caspase 9的活性,AKBA以剂量依赖的方式激活了Caspase 8和Caspase 9的产生。最后进行细胞期分布分析,流式细胞术分析显示,200 μg mL-1浓度的AKBA在G1期显著阻滞MCF-7细胞并引发细胞凋亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Antiproliferative and cell cycle arrest potentials of 3-O-acetyl-11-keto-β-boswellic acid against MCF-7 cells in vitro.

Introduction: Cancer is a major issue in medical science with increasing death cases every year worldwide. Therefore, searching for alternatives and nonorthodox methods of treatments with high efficiency, selectivity and less toxicity is the main goal in fighting cancer. Acetyl-11-keto-β-boswellic acid (AKBA), is a derivative pentacyclic triterpenoid that exhibited various biological activities with potential anti-tumoral agents. In this research, AKBA was utilized to examine the potential cytotoxic activity against MCF-7 cells in vitro and monitor the cellular and morphological changes with a prospective impact on apoptosis induction.

Methods: The cytotoxic activity of AKBA was measured by 3(4,5dimethylthiazole- 2-yl)-2,5 diphyneltetrazolium bromide (MTT) assay. A dose-dependent inhibition in MCF-7 cell viability was detected. The clonogenicity of MCF-7 cells was significantly suppressed by AKBA increment in comparison with untreated cells.

Result: Morphologically, exposure of MCF-7 cells to high AKBA concentrations caused changes in cell nuclear morphology which was indicated by increasing in nuclear size and cell permeability intensity. The mitochondrial membrane potential (ΔΨm) was reduced by increasing AKBA concentration with a significant release of cytochrome c. Acridine orange/ethidium bromide dual staining experiment confirmed that MCF-7 cells treated with AKBA (IC50 concentration) displayed a late stage of apoptosis indicated by intense and bright reddish colour.

Conclusion: A significant increase in reactive oxygen species formation was observed. Caspase 8 and caspase 9 activities were estimated and AKBA activated the production of caspase 8 and caspase 9 in a dose-dependent pattern. Finally, the cell phase distribution analysis was conducted, and flow cytometric analysis showed that AKBA at 200 μg mL-1 significantly arrest MCF-7 cells at the G1 phase and triggered apoptosis.

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