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当归甲醇提取物诱导人恶性脑肿瘤细胞凋亡并抑制肿瘤生长。

The Methanol Extract of Angelica sinensis Induces Cell Apoptosis and Suppresses Tumor Growth in Human Malignant Brain Tumors.

机构信息

College of Biological Science and Technology, National Chiao Tung University, Hsinchu 30010, Taiwan ; Center for Bioinformatics Research, National Chiao Tung University, Hsinchu 30010, Taiwan.

出版信息

Evid Based Complement Alternat Med. 2013;2013:394636. doi: 10.1155/2013/394636. Epub 2013 Nov 10.

DOI:10.1155/2013/394636
PMID:24319475
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3844186/
Abstract

Glioblastoma multiforme (GBM) is a highly vascularized and invasive neoplasm. The methanol extract of Angelica sinensis (AS-M) is commonly used in traditional Chinese medicine to treat several diseases, such as gastric mucosal damage, hepatic injury, menopausal symptoms, and chronic glomerulonephritis. AS-M also displays potency in suppressing the growth of malignant brain tumor cells. The growth suppression of malignant brain tumor cells by AS-M results from cell cycle arrest and apoptosis. AS-M upregulates expression of cyclin kinase inhibitors, including p16, to decrease the phosphorylation of Rb proteins, resulting in arrest at the G0-G1 phase. The expression of the p53 protein is increased by AS-M and correlates with activation of apoptosis-associated proteins. Therefore, the apoptosis of cancer cells induced by AS-M may be triggered through the p53 pathway. In in vivo studies, AS-M not only suppresses the growth of human malignant brain tumors but also significantly prolongs patient survival. In addition, AS-M has potent anticancer effects involving cell cycle arrest, apoptosis, and antiangiogenesis. The in vitro and in vivo anticancer effects of AS-M indicate that this extract warrants further investigation and potential development as a new antibrain tumor agent, providing new hope for the chemotherapy of malignant brain cancer.

摘要

多形性胶质母细胞瘤(GBM)是一种高度血管化和侵袭性的肿瘤。当归甲醇提取物(AS-M)在传统中药中常用于治疗多种疾病,如胃黏膜损伤、肝损伤、更年期症状和慢性肾小球肾炎。AS-M 还显示出抑制恶性脑肿瘤细胞生长的能力。AS-M 抑制恶性脑肿瘤细胞的生长是通过细胞周期停滞和细胞凋亡实现的。AS-M 上调细胞周期蛋白激酶抑制剂的表达,包括 p16,从而减少 Rb 蛋白的磷酸化,导致细胞停滞在 G0-G1 期。AS-M 增加 p53 蛋白的表达,并与凋亡相关蛋白的激活相关。因此,AS-M 诱导的癌细胞凋亡可能是通过 p53 途径触发的。在体内研究中,AS-M 不仅抑制人恶性脑肿瘤的生长,而且显著延长患者的生存时间。此外,AS-M 具有有效的抗癌作用,包括细胞周期停滞、凋亡和抗血管生成。AS-M 的体外和体内抗癌作用表明,这种提取物值得进一步研究和潜在开发作为一种新的抗脑肿瘤药物,为恶性脑癌的化疗提供了新的希望。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a9e/3844186/9ad8d9db8cdc/ECAM2013-394636.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a9e/3844186/d9f8e18f0563/ECAM2013-394636.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a9e/3844186/dbe33c7c1542/ECAM2013-394636.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a9e/3844186/d19a54edc51c/ECAM2013-394636.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a9e/3844186/75bafefe3f71/ECAM2013-394636.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a9e/3844186/9ad8d9db8cdc/ECAM2013-394636.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a9e/3844186/d9f8e18f0563/ECAM2013-394636.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a9e/3844186/dbe33c7c1542/ECAM2013-394636.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a9e/3844186/d19a54edc51c/ECAM2013-394636.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a9e/3844186/75bafefe3f71/ECAM2013-394636.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a9e/3844186/9ad8d9db8cdc/ECAM2013-394636.005.jpg

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