scholarly journals Nanoparticle Conjugation of Ginsenoside Rg3 Inhibits Hepatocellular Carcinoma Development and Metastasis

Small ◽  
2019 ◽  
Vol 16 (2) ◽  
pp. 1905233 ◽  
Author(s):  
Zhigang Ren ◽  
Xinmei Chen ◽  
Liangjie Hong ◽  
Xiaoxiong Zhao ◽  
Guangying Cui ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Ginsenoside Rg3 ◽  
Nanoparticle Conjugation

scholarly journals 20(S)-Ginsenoside Rg3 is a novel inhibitor of autophagy and sensitizes hepatocellular carcinoma to doxorubicin

Oncotarget ◽  
2014 ◽  
Vol 5 (12) ◽  
pp. 4438-4451 ◽  
Author(s):  
Dong-Gun Kim ◽  
Kyung Hee Jung ◽  
Da-Gyum Lee ◽  
Jung-Ho Yoon ◽  
Kyeong Sook Choi ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Ginsenoside Rg3

scholarly journals Liposomes co-loaded with ursolic acid and ginsenoside Rg3 in the treatment of hepatocellular carcinoma

2021 ◽  
Author(s):  
Bin Wang ◽  
Qiaoqiao Xu ◽  
Chenjian Zhou ◽  
Yu Lin
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Ursolic Acid ◽  
In Vitro Release ◽  
Entrapment Efficiency ◽  
Ginsenoside Rg3 ◽  
In Vitro Drug Release ◽  
Slowing Down ◽  
Mtt Method

Objective: Liposomes co-loaded with ursolic acid and ginsenoside Rg3 (UA+Rg3-LIP) were prepared to study their effects on the proliferation, apoptosis and cell cycle of hepatocellular carcinoma (HCC) cells. Methods: Liposomes were prepared by reverse evaporation, and then UA+Rg3-LIP were prepared by the pH gradient method, and followed by liposome characterization. Next, the effects of UA+Rg3-LIP on the proliferation, apoptosis and cell cycle of HepG2 cells were investigated by MTT method and flow cytometry at the cell level. Results: The entrapment efficiency of UA in UA+Rg3-LIP was 78.52% and that of Rg3 was 71.68%, as assayed by low-temperature ultracentrifugation. The in vitro release rates of UA+Rg3-LIP and UA+Rg3 detected by the dialysis membrane method were 1–10 h. The release rate of UA+Rg3 was close to 100%; that of UA+Rg3-LIP was decreased after 10 h and approached 100% after 24 h. It was further confirmed by cell experiments that UA+Rg3-LIP could significantly reduce cells' viability while at the same time increase their apoptosis rate and raise the proportion of cells in the G0/G1 phase. Conclusion: Liposomes co-loaded with ursolic acid and ginsenoside Rg3 could affect cell proliferation, apoptosis and cell cycle, thus slowing down the in vitro drug release ability of HCC.

scholarly journals Ginsenoside Rg3 Prolongs Survival of the Orthotopic Hepatocellular Carcinoma Model by Inducing Apoptosis and Inhibiting Angiogenesis

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Shen Hu ◽  
Yan Zhu ◽  
Xiangyang Xia ◽  
Xiaobo Xu ◽  
Fen Chen ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Microvessel Density ◽  
Tumor Model ◽  
Oral Feeding ◽  
Apoptosis Induction ◽  
Ginsenoside Rg3 ◽  
Kaplan Meier ◽  
Induced Apoptosis

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 (n=10) were compared with the control (n=10) 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 (P<0.05). Rg3-treated mice showed a longer survival than the control (P<0.05). 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.

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