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Xu X.-H.,University of South China | He J.-B.,Huaihua First Peoples Hospital | Zhang P.,University of South China
Chinese Journal of Cancer Prevention and Treatment | Year: 2013

OBJECTIVE: To evaluate the inhibitory efficacy of the combination of Ginsenoside Rg3 and Suramin on the growth of the Lewis lung cancer in mice. METHODS: Forty C57BL6 mice bearing Lewis lung carcinoma were randomized into several groups, and received cisplatin 3 mg/(kg·5 d), ginsenoside Rg3 5 mg/(kg·d), suramin 10 mg/(kg·d), ginsenoside Rg3 combined with suramin therapy respectively for 16 days. The transplanted tumor weight and the tumor inhibiting rate were measured in every group. The tumor microvascular density (MVD) was detected by immunohistochemistry, and the expression of MEK1/2, ERK1/2, and p-ERK1/2 were detected by RT-PCR and western blot. RESULTS: After treated with cisplatin, suramin, ginsenoside Rg3, ginsenoside Rg3 combined with suramin respectively, the growth of transplanted tumor was inhibited markedly. The tumor inhibitory rate was 19.7%, 35.4%, 35.9% and 49.4% in the cisplatin, suramin, ginsenoside Rg3, ginsenoside Rg3 combined with suramin therapy group respectively. In the control group, and every therapy group, the expression of MVD were 24.06±2.40, 19.41±1.98, 13.06±1.92, 12.09±1.49 and 6.16±1.17, respectively. The ERK1/2mRNA were (71.93±13.47)%, (56.43±11.01)%, (45.27±8.82)%, (43.29±7.48)% and (28.75±5.41)%, respectively. The ERK1/2 protein were (104.18±9.78)%, (84.61±7.66)%, (76.71±7.25)%, (74.01±7.41)% and (51.69±5.29)%, respectively, and the p-ERK1/2 protein were (112.96±9.49)%, (87.86±6.77)%, (61.26±8.48)%, (38.60±10.66)% and (9.57±3.42)%, respectively. The MVD was decreased significantly in therapy groups, especially in the combination group (P<0.01). Compared with the control group, the expression of the ERK1/2 and p-ERK1/2 was down-regulated in the four therapy groups, and especially in the combination group whether at the mRNA or protein level (P<0.01). CONCLUSION: The results indicates that Suramin combined with Ginsenoside Rg3 can inhibite the growth of Lewis lung cancer more effectively in mice, which possibly is related to inhibite the angiogenesis via suppressing the Extracellular Signal Kinase Pathway. Source


He J.-B.,Huaihua First Peoples Hospital | Liao H.-Z.,Huaihua First Peoples Hospital | Yi G.-Z.,Huaihua First Peoples Hospital | Chen Z.-K.,Huaihua First Peoples Hospital | He W.,Huaihua First Peoples Hospital
Tumor | Year: 2012

Objective: To investigate the inhibitory effects of ginsenoside Rg3 on the growth and metastasis of lung carcinoma allografts in mice, and to explore the possible mechanism. Methods: The mice bearing a metastatic variant of Lewis lung carcinoma were established, and then they were randomized to receive 0.9% sodium chloride solution (as a control), DDP (cisplatin), and ginsenoside Rg3 from the fourth day after transplant, respectively. Until the twenty-fourth day after transplant, the mice were sacrificed. The subcutaneous tumor was dissected, and the lung was removed. The inhibitory rate of tumor growth and the number of metastatic foci on the lung surface were counted. The expressions of SSTR (somatostatin receptor), VEGF (vascular endothelial growth factor) and PCNA (proliferation cell nuclear antigen) in subcutaneous tumor were examined by immunohistochemistry. The apoptosis was detected by TUNEL (terminal transferase-mediated dUTP nick end-labeling) method. Results: The inhibitory rates of tumor growth in DDP-treated group and the ginsenoside Rg3-treated group were 39.20% and 54.86%, respectively (P < 0.01). The numbers of metastatic foci on the lung surface in DDP-treated group and the ginsenoside Rg3-treated group were decreased by 30.25% and 58.57%, respectively (P < 0.05). The expression level of SSTR and the apoptosis index in the ginsenoside Rg3- treated group were higher than those in the control group and the DDP-treated group (P < 0.01), while the expression level of VEGF and the proliferation index of PCNA in the ginsenoside Rg3-treated group were decreased as compared with the control group and the DDP-treated group (P < 0.01, P < 0.05). Conclusion: Ginsenoside Rg3 can inhibit the growth and metastasis of lung carcinoma allografts in mice. The mechanism may be associated with the overexpression of SSTR. Copyright © 2012 by TUMOR. Source

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