[Antiangiogenesis of ginsenoside Rg3 in severe combined immunodeficient mice with human ovarian carcinoma].
Zimin Pan, Da-feng Ye, Xing Xie, Huaizeng Chen, Weiguo Lü
Abstract
Zimin Pan, Da-feng Ye, Xing Xie, Huaizeng Chen, Weiguo Lü
Abstract
OBJECTIVE: To investigate the antiangiogenesis of ginsenoside Rg3 in severe combined immunodeficient (SCID) mice with human ovarian carcinoma by detecting vascular endothelial growth factor (VEGF) mRNA, VEGF protein level and microvascular density (MVD). METHODS: The SCID mice with human ovarian carcinoma SKOV3 cells were treated with Rg3 (300 microgram 400 microl(-1) mouse(-1)), mice with phosphate buffered solution (PBS) and without Rg3 and PBS were used as control. Tumor volume, metastasis, ascites, VEGF mRNA, VEGF protein and MVD were detected. The level of VEGF mRNA in tumor tissue was determined by relative quantative reverse transcription polymerase chain reaction. VEGF protein level in sera and ascitic fluids were determined by enzyme-linked immunosorbent assay. MVD was calculated by immunohistochemistry (anti-CD34). RESULTS: (1) No ascites was formed and the size of metastasis decreased in SKOV3/Rg3 group. (2) Expression of VEGF mRNA level in SKOV3/Rg3 group (119 +/- 16) was lower significantly than those of the control groups (254 +/- 4, 273 +/- 44, respectively, P < 0.05). (3) Serum VEGF level in SKOV3/Rg3 group [(14.6 +/- 0.7) pg/ml] was lower significantly than those of SKOV3 group and SKOV3/PBS group [(18.5 +/- 2.1) and (20.5 +/- 1.7) pg/ml, respectively, P < 0.05]. (4) MVD in tumor tissues of SKOV3/Rg3 group (43 +/- 7) was lower than that of each control group (65 +/- 12, 73 +/- 10, respectively, P < 0.05). CONCLUSION: Ginsenoside Rg3 can block angiogenesis and inhibit tumor growth and metastasis by down regulating the expression of VEGF mRNA and protein and reducing microvascular density.
OpenAlex reports 7 citations for this work. Citation counts describe recorded attention and do not establish research quality.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
OBJECTIVE: To investigate the antiangiogenesis of ginsenoside Rg3 in severe combined immunodeficient (SCID) mice with human ovarian carcinoma by detecting vascular endothelial growth factor (VEGF) mRNA, VEGF protein level and microvascular density (MVD). METHODS: The SCID mice with human ovarian carcinoma SKOV3 cells were treated with Rg3 (300 microgram 400 microl(-1) mouse(-1)), mice with phosphate buffered solution (PBS) and without Rg3 and PBS were used as control. Tumor volume, metastasis, ascites, VEGF mRNA, VEGF protein and MVD were detected. The level of VEGF mRNA in tumor tissue was determined by relative quantative reverse transcription polymerase chain reaction. VEGF protein level in sera and ascitic fluids were determined by enzyme-linked immunosorbent assay. MVD was calculated by immunohistochemistry (anti-CD34). RESULTS: (1) No ascites was formed and the size of metastasis decreased in SKOV3/Rg3 group. (2) Expression of VEGF mRNA level in SKOV3/Rg3 group (119 +/- 16) was lower significantly than those of the control groups (254 +/- 4, 273 +/- 44, respectively, P < 0.05). (3) Serum VEGF level in SKOV3/Rg3 group [(14.6 +/- 0.7) pg/ml] was lower significantly than those of SKOV3 group and SKOV3/PBS group [(18.5 +/- 2.1) and (20.5 +/- 1.7) pg/ml, respectively, P < 0.05]. (4) MVD in tumor tissues of SKOV3/Rg3 group (43 +/- 7) was lower than that of each control group (65 +/- 12, 73 +/- 10, respectively, P < 0.05). CONCLUSION: Ginsenoside Rg3 can block angiogenesis and inhibit tumor growth and metastasis by down regulating the expression of VEGF mRNA and protein and reducing microvascular density.
Key concepts: Ovarian carcinoma, Vascular endothelial growth factor, Angiogenesis, Ovarian cancer, Ascites, Metastasis, Immunohistochemistry, Messenger RNA