Anti-angiogenic effects of zengmian YiIiu granule on ovarian carcinoma xenograft.
- Author:
Xin-Xin HU
1
;
Qin-Hua ZHANG
;
Cong QI
Author Information
- Publication Type:Journal Article
- MeSH: Angiogenesis Inhibitors; pharmacology; Animals; Cell Line, Tumor; Drugs, Chinese Herbal; pharmacology; Female; Humans; Hypoxia-Inducible Factor 1, alpha Subunit; metabolism; Mice; Mice, Inbred BALB C; Neoplasms, Glandular and Epithelial; blood supply; drug therapy; Neovascularization, Pathologic; prevention & control; Ovarian Neoplasms; blood supply; drug therapy; Vascular Endothelial Growth Factor A; metabolism; Vascular Endothelial Growth Factor Receptor-2; metabolism; Xenograft Model Antitumor Assays
- From: Chinese Journal of Integrated Traditional and Western Medicine 2012;32(7):970-974
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the anti-angiogenic effects and mechanisms of Zengmian Yiliu Granule (ZMYLG) on ovarian carcinoma xenograft.
METHODSThe SKOV3 ovarian carcinoma bearing mouse model was established. The tumor-bearing mice were randomly divided into the control group, the paclitaxel group, the high, medium, and low dose ZMYLG group, 8 in each group. The medication was lasted for ten days. The microvessel density (MVD) in the xenograft was calculated by the method of using cell membrane differentiation antigen 34 (CD34) antibody marking new vascular endothelial cells. The protein and mRNA expressions of vascular endothelial growth factor (VEGF) and its receptor fetal liver kinase-1 (FLK-1), hypoxia inducible factor-1alpha (HIF-1alpha) in the tumor were determined using immunohistochemical assay and RT-PCR.
RESULTSThe MVD of ovarian carcinoma xenografts in the paclitaxel group, the high, medium, and low dose ZMYLG group obviously decreased, showing statistical difference when compared with the control group (P < 0.01, P < 0.05). Each ZMYLG dose group could down-regulate the protein and mRNA expressions of VEGF, FLK-1, and HIF-1alpha (P < 0.01, P < 0.05).
CONCLUSIONSZMYLG could inhibit neogenesis of tumor vessels. Its mechanisms might be associated with down-regulating the expression of HIF-1alpha, modifying the hypoxic state, inhibiting the expressions of VEGF and FLK-1, and exerting its anti-angiogenic effects.
