Gambogenic acid inhibits proliferation of A549 cells through apoptosis-inducing.
- Author:
Li YANG
1
;
Mei WANG
;
Hui CHENG
;
Qinglin LI
Author Information
1. Experimental Center for Scientific Research, Anhui University of Traditional Chinese Medicine, Hefei 230038, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Antineoplastic Agents, Phytogenic;
therapeutic use;
Apoptosis;
drug effects;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Cyclooxygenase 2;
metabolism;
Humans;
Immunohistochemistry;
In Situ Nick-End Labeling;
Lung Neoplasms;
drug therapy;
metabolism;
ultrastructure;
Male;
Mice;
Mice, Inbred BALB C;
Mice, Nude;
Microscopy, Electron, Transmission;
Terpenes;
therapeutic use;
Vascular Endothelial Growth Factor A;
metabolism;
Xanthenes;
Xanthones;
therapeutic use;
Xenograft Model Antitumor Assays
- From:
China Journal of Chinese Materia Medica
2011;36(9):1217-1221
- CountryChina
- Language:Chinese
-
Abstract:
To explore gambogenic acid (GNA)-induced apoptosis and underlying mechanism in vivo. A549 nude mice xenografts were used as in vivo model to study anticancer effect of GNA by observing tumor growth curve and weight of the tumor. Ultrastructure of A549 cells treated by GNA was observed by TE. Expression of COX-2 and VEGF were detected by immunohistochemistry. TUNEL assay was applied in examining apoptosis index of tumor cells. The tumor isolated from mice treated by GNA (8, 16 mg kg(-1)) took on a slow growth condition compared with control group. The results suggested that weight and volume of the tumor from experimental groups were remarkably decreased compared with control group (P < 0.05). Ultrastructure change of the tumor, such as vacuolization, abnormal distribution of the heterochromosome, volume of the tumor cells, even apoptotic bodies, were observed in GNA-treated group. While no apparent morphological change was observed in the normal group. Typical apoptotic characteristics could be distinctly observed in the mouse treated by GNA for 20 days and apoptosis index in GNA-treated group was significantly higher than model group. Expression of COX-2 and VEGF were significantly down-regulated in GNA-treated groups in comparison with control group (P < 0.01). These results indicate that GNA could affect the development and progression of A549 cells through inducing apoptosis, mediating the expression of VEGF in vascular cells and COX-2 in tumor cells.
