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Ginsenoside Rg3 Prolongs Survival of the Orthotopic Hepatocellular Carcinoma Model by Inducing Apoptosis and Inhibiting Angiogenesis.
Analytical Cellular Pathology ( IF 2.6 ) Pub Date : 2019-08-26 , DOI: 10.1155/2019/3815786
Shen Hu 1 , Yan Zhu 2 , Xiangyang Xia 3 , Xiaobo Xu 4 , Fen Chen 4 , Xudong Miao 5 , Xinmei Chen 6
Affiliation  

Aim. Microvessel density is a marker of tumor angiogenesis activity for development and metastasis. Our preliminary study showed that ginsenoside Rg3 (Rg3) induces apoptosis in hepatocellular carcinoma (HCC) in vitro. The aim of this study was to investigate the cross-link for apoptosis induction and antiangiogenesis effect of Rg3 on orthotopic HCC in vivo. Methods. The murine HCC cells Hep1-6 were implanted in the liver of mouse. With oral feeding of Rg3 (10 mg/kg once a day for 30 days), the quantitative analysis of apoptosis was performed by using pathology and a transmission electron microscope and microvessel density was quantitatively measured by immunohistochemical staining of the CD105 antibody. The mice treated with Rg3 () were compared with the control () using Kaplan-Meier analysis. Animal weight and tumor weight were measured to determine the toxicity of Rg3 and antitumor effect on an orthotopic HCC tumor model. Results. With oral feeding of Rg3 daily in the first 30 days on tumor implantation, Rg3 significantly decreased the orthotopic tumor growth and increased the survival of animals (). Rg3-treated mice showed a longer survival than the control (). Rg3 treatment induced apoptosis and inhibited angiogenesis. They contributed to the tumor shrinkage. Rg3 initialized the tumor apoptotic progress, which then weakened the tumor volume and its capability to produce the vascularized network for further growth of the tumor and remote metastasis. Conclusion. Rg3 inhibited the activation of microtumor vessel formation in vivo besides its apoptosis induction. Rg3 may be used as an adjuvant agent in the clinical HCC treatment regimen.

中文翻译:

人参皂甙 Rg3 通过诱导细胞凋亡和抑制血管生成来延长原位肝细胞癌模型的生存期。

瞄准。微血管密度是肿瘤血管生成活动发展和转移的标志。我们的初步研究表明,人参皂苷 Rg3 (Rg3)在体外诱导肝细胞癌 (HCC) 细胞凋亡。本研究的目的是研究 Rg3在体内对原位 HCC 的细胞凋亡诱导和抗血管生成作用的交联。方法。将小鼠HCC细胞Hep1-6植入小鼠肝脏。口服Rg3(10mg/kg,每天1次,共30天),通过病理学和透射电子显微镜进行细胞凋亡的定量分析,通过CD105抗体的免疫组织化学染色定量测量微血管密度。用 Rg3 处理的小鼠 ()与对照 ()使用 Kaplan-Meier 分析。测量动物体重和肿瘤重量以确定 Rg3 的毒性和对原位 HCC 肿瘤模型的抗肿瘤作用。结果。在肿瘤植入后的前 30 天每天口服 Rg3,Rg3 显着降低原位肿瘤的生长并提高动物的存活率。)。Rg3 处理的小鼠比对照组的存活时间更长()。Rg3 处理诱导细胞凋亡并抑制血管生成。它们促成了肿瘤缩小。Rg3 启动了肿瘤的凋亡进程,从而削弱了肿瘤体积及其产生血管化网络以促进肿瘤进一步生长和远处转移的能力。结论。除了诱导细胞凋亡外,Rg3 还抑制体内微肿瘤血管形成的激活。Rg3可用作临床HCC治疗方案中的辅助剂。
更新日期:2019-08-26
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