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Osbeckia octandra 的叶提取物诱导口腔鳞状细胞癌细胞凋亡。

Leaf extract of Osbeckia octandra induces apoptosis in oral squamous cell carcinoma cells.

机构信息

Oral Cancer Research Institute, Department of Oral Pathology, Yonsei University College of Dentistry, Seoul, 03722, Republic of Korea.

Department of Obstetrics and Gynecology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, 06230, Republic of Korea.

出版信息

BMC Complement Med Ther. 2022 Jan 25;22(1):20. doi: 10.1186/s12906-022-03505-4.

DOI:10.1186/s12906-022-03505-4
PMID:35078428
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8787916/
Abstract

BACKGROUND

Osbeckia octandra is a plant endemic to Sri Lanka and is used in ethnomedicine for treating various diseases. However, the anti-cancer properties of O. octandra are yet to be fully investigated. In the present study, we evaluated the anti-cancer effects of O. octandra on oral cancer cells.

METHODS

Human oral cancer cell lines (HSC2, YD10B, YD38, YD9, and YD32) were used in this study. BrdU incorporation, cell cycle and annexin-V/PI staining were all evaluated using flow cytometry to determine the extent to which O. octandra leaf extract inhibits cell proliferation and induces apoptosis. Cell viability and reactive oxygen species (ROS) were also measured in order to investigate the anti-cancer effects of O. octandra extracts. Western blotting was performed to detect cell cycle related protein such as cyclin d1 and cdk4, and to detect apoptosis-related proteins such as Bcl-2, Bcl-X, Bax, Caspase-9, Cleaved caspase-3, Fas, Caspase-8, and Bid.

RESULTS

Leaf extract of O. octandra reduced oral squamous cell carcinoma (OSCC) cell viability in a dose-dependent manner. Leaf extract of O. octandra has non-toxic in normal keratinocytes. Also, O. octandra extract interrupted the DNA replication via G1 phase arrests, and this effect was independent of ROS generation. In the apoptosis-related experiments, the population of annexin V-positive cells increased upon treatment with O. octandra extract. Furthermore, the expression of anti-apoptotic protein (Bcl-2 and Bcl-xL) was decreased, whereas the expression of cleaved caspase-3 protein was increased in O. octandra-treated OSCC cells.

CONCLUSIONS

The results suggest that a leaf extract of O. octandra inhibited the proliferation of OSCC cells through G phase arrest and interrupting DNA replication. The leaf extract of O. octandra could trigger the apoptotic response via caspase 3 activation in OSCC cells. These results suggest that O. octandra has the potential to be developed as an alternative medicine for treating OSCC.

摘要

背景

Osbeckia octandra 是斯里兰卡特有的植物,在传统医学中用于治疗各种疾病。然而,Osbeckia octandra 的抗癌特性尚未得到充分研究。本研究评估了 Osbeckia octandra 叶提取物对口腔癌细胞的抗癌作用。

方法

本研究使用人口腔癌细胞系(HSC2、YD10B、YD38、YD9 和 YD32)。通过 BrdU 掺入、细胞周期和 Annexin-V/PI 染色的流式细胞术评估,确定 Osbeckia octandra 叶提取物抑制细胞增殖和诱导细胞凋亡的程度。还测量了细胞活力和活性氧 (ROS),以研究 Osbeckia octandra 提取物的抗癌作用。进行 Western blot 以检测细胞周期相关蛋白,如 cyclin d1 和 cdk4,以及检测凋亡相关蛋白,如 Bcl-2、Bcl-X、Bax、Caspase-9、Cleaved caspase-3、Fas、Caspase-8 和 Bid。

结果

Osbeckia octandra 叶提取物以剂量依赖的方式降低口腔鳞状细胞癌 (OSCC) 细胞活力。Osbeckia octandra 叶提取物对正常角质形成细胞无毒。此外,Osbeckia octandra 提取物通过 G1 期阻滞干扰 DNA 复制,这种作用与 ROS 产生无关。在凋亡相关实验中,用 Osbeckia octandra 提取物处理后, Annexin V 阳性细胞的比例增加。此外,在 Osbeckia octandra 处理的 OSCC 细胞中,抗凋亡蛋白(Bcl-2 和 Bcl-xL)的表达减少,而 cleaved caspase-3 蛋白的表达增加。

结论

结果表明,Osbeckia octandra 叶提取物通过 G 期阻滞和中断 DNA 复制抑制 OSCC 细胞增殖。Osbeckia octandra 叶提取物可通过 caspase 3 激活在 OSCC 细胞中引发凋亡反应。这些结果表明,Osbeckia octandra 有可能被开发为治疗 OSCC 的替代药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d80f/8787916/47aa8d35b554/12906_2022_3505_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d80f/8787916/572d84f44ccf/12906_2022_3505_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d80f/8787916/037a98b86f44/12906_2022_3505_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d80f/8787916/0620b79ed4ad/12906_2022_3505_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d80f/8787916/47aa8d35b554/12906_2022_3505_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d80f/8787916/572d84f44ccf/12906_2022_3505_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d80f/8787916/037a98b86f44/12906_2022_3505_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d80f/8787916/0620b79ed4ad/12906_2022_3505_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d80f/8787916/47aa8d35b554/12906_2022_3505_Fig4_HTML.jpg

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