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大麻二酚而非大麻提取物可抑制宫颈癌细胞的生长并诱导其凋亡。

Cannabidiol rather than Cannabis sativa extracts inhibit cell growth and induce apoptosis in cervical cancer cells.

作者信息

Lukhele Sindiswa T, Motadi Lesetja R

机构信息

Department of Biochemistry, North-west University (Mafikeng campus), Private Bag X1290, Potchefstroom, 2520, South Africa.

出版信息

BMC Complement Altern Med. 2016 Sep 1;16(1):335. doi: 10.1186/s12906-016-1280-0.

DOI:10.1186/s12906-016-1280-0
PMID:27586579
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5009497/
Abstract

BACKGROUND

Cervical cancer remains a global health related issue among females of Sub-Saharan Africa, with over half a million new cases reported each year. Different therapeutic regimens have been suggested in various regions of Africa, however, over a quarter of a million women die of cervical cancer, annually. This makes it the most lethal cancer amongst black women and calls for urgent therapeutic strategies. In this study we compare the anti-proliferative effects of crude extract of Cannabis sativa and its main compound cannabidiol on different cervical cancer cell lines.

METHODS

To achieve our aim, phytochemical screening, MTT assay, cell growth analysis, flow cytometry, morphology analysis, Western blot, caspase 3/7 assay, and ATP measurement assay were conducted.

RESULTS

Results obtained indicate that both cannabidiol and Cannabis sativa extracts were able to halt cell proliferation in all cell lines at varying concentrations. They further revealed that apoptosis was induced by cannabidiol as shown by increased subG0/G1 and apoptosis through annexin V. Apoptosis was confirmed by overexpression of p53, caspase 3 and bax. Apoptosis induction was further confirmed by morphological changes, an increase in Caspase 3/7 and a decrease in the ATP levels.

CONCLUSIONS

In conclusion, these data suggest that cannabidiol rather than Cannabis sativa crude extracts prevent cell growth and induce cell death in cervical cancer cell lines.

摘要

背景

宫颈癌仍是撒哈拉以南非洲地区女性面临的一个全球健康相关问题，每年报告的新病例超过50万例。非洲不同地区已提出了不同的治疗方案，然而，每年仍有超过25万女性死于宫颈癌。这使其成为黑人女性中最致命的癌症，亟需治疗策略。在本研究中，我们比较了大麻粗提物及其主要化合物大麻二酚对不同宫颈癌细胞系的抗增殖作用。

方法

为实现我们的目标，进行了植物化学筛选、MTT 试验、细胞生长分析、流式细胞术、形态学分析、蛋白质免疫印迹法、半胱天冬酶3/7试验和ATP测量试验。

结果

获得的结果表明，大麻二酚和大麻提取物在不同浓度下均能使所有细胞系的细胞增殖停止。结果还显示，大麻二酚可诱导细胞凋亡，表现为亚G0/G1期增加以及膜联蛋白V介导的凋亡。p53、半胱天冬酶3和bax的过表达证实了细胞凋亡。形态学变化、半胱天冬酶3/7增加和ATP水平降低进一步证实了细胞凋亡的诱导。

结论

总之，这些数据表明，在宫颈癌细胞系中，大麻二酚而非大麻粗提物可阻止细胞生长并诱导细胞死亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/eab1e360e3f2/12906_2016_1280_Fig12_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/30b17d6ec76f/12906_2016_1280_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/4e6cbd7b2cf2/12906_2016_1280_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/44f1503a56e1/12906_2016_1280_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/b5fa01a95529/12906_2016_1280_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/bfd41c1ecf1a/12906_2016_1280_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/b262b3010fcc/12906_2016_1280_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/77340038ae44/12906_2016_1280_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/de0e9d7f300f/12906_2016_1280_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/13d5f7a022fd/12906_2016_1280_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/f80fdcc546b7/12906_2016_1280_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/a429cc350719/12906_2016_1280_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/eab1e360e3f2/12906_2016_1280_Fig12_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/30b17d6ec76f/12906_2016_1280_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/4e6cbd7b2cf2/12906_2016_1280_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/44f1503a56e1/12906_2016_1280_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/b5fa01a95529/12906_2016_1280_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/bfd41c1ecf1a/12906_2016_1280_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/b262b3010fcc/12906_2016_1280_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/77340038ae44/12906_2016_1280_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/de0e9d7f300f/12906_2016_1280_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/13d5f7a022fd/12906_2016_1280_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/f80fdcc546b7/12906_2016_1280_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/a429cc350719/12906_2016_1280_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4867/5009497/eab1e360e3f2/12906_2016_1280_Fig12_HTML.jpg

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