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绿原酸诱导结直肠癌细胞凋亡和细胞周期停滞。

Chlorogenic acid induces apoptosis and cell-cycle arrest in colorectal cancer cells.

机构信息

Department of Microbiology and Immunology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran.

Department of Immunology and Oncology, Faculty of Veterinary Medicine, Islamic Azad University-Garmsar Branch, Garmsar, Iran.

出版信息

Mol Biol Rep. 2023 Dec;50(12):9845-9857. doi: 10.1007/s11033-023-08854-y. Epub 2023 Oct 17.

DOI:10.1007/s11033-023-08854-y
PMID:37847443
Abstract

BACKGROUND

Apoptotic agents from natural products like phenolic compounds can be used effectively in the treatment of cancer. Chlorogenic acid (CGA) is one of the phenolic compounds in medicinal plants with anti-cancer properties. In this research, we aimed to explore the anti-cancer mode of action of CGA on colorectal cancer (CRC) cells in vitro conditions.

METHODS

HT-29 and HEK-293 cells were cultured after MTT assay for 24 h with CGA 100 µM, and without CGA. Then, flow cytometry assays and the expression of apoptosis-related genes including caspase 3 and 9, Bcl-2 and Bax, and cell cycle-related genes including P21, P53 and NF-κB at mRNA and protein levels were examined. Finally, we measured the amount of intracellular reactive oxygen species (ROS).

RESULTS

The cell viability of all two-cell lines decreased in a dose-dependent manner. Moreover, CGA induces cell cycle arrest in HT-29 cells by increasing the expression of P21 and P53. It also induces apoptosis in HT-29 cells by mitigating Bcl-2 and NF-κB expression and elevating caspase 3 and 9 expression and ROS levels.

CONCLUSIONS

Considering the cytotoxicity and cell cycle arrest and induction of apoptosis in the colon cancer cell line by CGA, it can be concluded that CGA is a suitable option for the treatment of colon cancer.

摘要

背景

天然产物中的凋亡剂,如酚类化合物,可以有效地用于癌症治疗。绿原酸(CGA)是具有抗癌特性的药用植物中的酚类化合物之一。在这项研究中,我们旨在探讨 CGA 在体外条件下对结直肠癌细胞(CRC)的抗癌作用模式。

方法

用 100µM CGA 处理 HT-29 和 HEK-293 细胞 24 小时后,通过 MTT 测定法进行培养,然后检查与凋亡相关的基因(包括 caspase 3 和 9、Bcl-2 和 Bax)和与细胞周期相关的基因(包括 P21、P53 和 NF-κB)在 mRNA 和蛋白水平上的表达以及细胞内活性氧(ROS)的含量。

结果

两种细胞系的细胞活力均呈剂量依赖性下降。此外,CGA 通过增加 P21 和 P53 的表达,诱导 HT-29 细胞周期停滞。它还通过减轻 Bcl-2 和 NF-κB 的表达以及增加 caspase 3 和 9 的表达和 ROS 水平,诱导 HT-29 细胞凋亡。

结论

考虑到 CGA 对结肠癌细胞系的细胞毒性、细胞周期停滞和诱导凋亡作用,可以得出结论,CGA 是治疗结肠癌的合适选择。

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