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黄芪甲苷诱导肝癌细胞凋亡、G1 期阻滞并抑制抗凋亡信号通路。

Astragaloside IV Induces Apoptosis, G-Phase Arrest and Inhibits Anti-apoptotic Signaling in Hepatocellular Carcinoma.

机构信息

Department of Surgery, Show Chwan Memorial Hospital, Changhua, Taiwan, R.O.C.

Emergency Department, Cathay General Hospital, Taipei, Taiwan, R.O.C.

出版信息

In Vivo. 2020 Mar-Apr;34(2):631-638. doi: 10.21873/invivo.11817.

DOI:10.21873/invivo.11817
PMID:32111763
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7157888/
Abstract

BACKGROUND/AIM: Hepatocellular carcinoma (HCC) is a primary malignancy of the liver and the third leading cause of cancer death worldwide. Although multiple chemotherapies options are available for HCC, chemo-induced toxicity is inevitable during clinical treatment. Therefore, identifying possible adjuvant agents with both liver-protective and antitumor effects is critical. Herbal medicines have chemopreventive and anti-HCC effect, such as Juzen taiho-to and Sho-saiko-to. Astragaloside IV is a compound extracted from the Chinese medical herb Astragalus membranaceus (Fisch.) Bge. with liver protection potential. However, whether astragaloside IV may also possess tumor-inhibitory capability and its underlying mechanism is remaining unknown.

MATERIALS AND METHODS

Viability analysis, cell-cycle analysis, apoptosis analysis, western blotting analysis and invasion trans-well assay were performed to identify tumor-inhibitory potential of astragaloside IV on HCC cells (SK-Hep1 and Hep3B cells).

RESULTS

We found that astragaloside IV may induce cytotoxicity and extrinsic/intrinsic apoptosis effect, but also trigger G arrest in HCC cells. The expression of anti-apoptotic proteins of HCC were all reduced by astragaloside IV. Additionally, astragaloside IV also suppressed HCC cell invasion ability.

CONCLUSION

Astragaloside IV effectively suppressed HCC cell proliferation, invasion and anti-apoptosis in vitro.

摘要

背景/目的:肝细胞癌(HCC)是肝脏的原发性恶性肿瘤,也是全球癌症死亡的第三大主要原因。尽管有多种化疗方案可用于 HCC,但在临床治疗中不可避免会发生化疗诱导的毒性。因此,寻找具有肝脏保护和抗肿瘤作用的可能辅助剂至关重要。草药具有化学预防和抗 HCC 作用,如 Juzen taiho-to 和 Sho-saiko-to。黄芪甲苷是从中药黄芪(Fisch.)Bge. 中提取的一种化合物,具有肝脏保护潜力。然而,黄芪甲苷是否也具有肿瘤抑制能力及其潜在机制尚不清楚。

材料和方法

通过活力分析、细胞周期分析、凋亡分析、Western blot 分析和侵袭 Trans-well 分析,鉴定黄芪甲苷对 HCC 细胞(SK-Hep1 和 Hep3B 细胞)的肿瘤抑制潜力。

结果

我们发现黄芪甲苷可能诱导 HCC 细胞的细胞毒性和外源性/内源性细胞凋亡作用,同时触发 G 期细胞阻滞。黄芪甲苷还降低了 HCC 细胞中抗凋亡蛋白的表达。此外,黄芪甲苷还抑制了 HCC 细胞的侵袭能力。

结论

黄芪甲苷在体外有效抑制 HCC 细胞的增殖、侵袭和抗凋亡。

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本文引用的文献

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Protein Kinase B and Extracellular Signal-Regulated Kinase Inactivation is Associated with Regorafenib-Induced Inhibition of Osteosarcoma Progression In Vitro and In Vivo.蛋白激酶B和细胞外信号调节激酶失活与瑞戈非尼诱导的骨肉瘤体外和体内进展抑制相关。
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Astragaloside IV protects against cisplatin-induced liver and kidney injury via autophagy-mediated inhibition of NLRP3 in rats.黄芪甲苷通过自噬介导的对大鼠NLRP3的抑制作用预防顺铂诱导的肝肾损伤。
J Toxicol Sci. 2019;44(3):167-175. doi: 10.2131/jts.44.167.
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CDK 4/6 Inhibitors as Single Agent in Advanced Solid Tumors.CDK 4/6抑制剂作为晚期实体瘤的单一药物治疗
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Magnolol Induces Apoptosis and Inhibits ERK-modulated Metastatic Potential in Hepatocellular Carcinoma Cells.厚朴酚诱导肝癌细胞凋亡并抑制ERK调节的转移潜能。
In Vivo. 2018 Nov-Dec;32(6):1361-1368. doi: 10.21873/invivo.11387.
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Astragaloside IV Attenuates Acetaminophen-Induced Liver Injuries in Mice by Activating the Nrf2 Signaling Pathway.黄芪甲苷通过激活 Nrf2 信号通路减轻对乙酰氨基酚诱导的小鼠肝损伤。
Molecules. 2018 Aug 14;23(8):2032. doi: 10.3390/molecules23082032.
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Amentoflavone enhances sorafenib-induced apoptosis through extrinsic and intrinsic pathways in sorafenib-resistant hepatocellular carcinoma SK-Hep1 cells .穗花杉双黄酮通过外源性和内源性途径增强索拉非尼诱导的索拉非尼耐药肝癌SK-Hep1细胞凋亡。
Oncol Lett. 2017 Sep;14(3):3229-3234. doi: 10.3892/ol.2017.6540. Epub 2017 Jul 8.
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Regorafenib Induces Apoptosis and Inhibits Metastatic Potential of Human Bladder Carcinoma Cells.瑞戈非尼诱导人膀胱癌细胞凋亡并抑制其转移潜能。
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