Inhibition of Jumi extraction on growth of human cervical cancer cell line HeLa.
- Author:
Wei KUANG
1
;
Hui-Ling CHEN
;
Jian-Ping JIANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Caspase 3; metabolism; Caspase 6; metabolism; Caspase 7; metabolism; Cell Proliferation; drug effects; Chrysanthemum; Female; HeLa Cells; Humans; Mice; Mice, Inbred BALB C; Mice, Nude; Plant Extracts; pharmacology; Xenograft Model Antitumor Assays
- From: Chinese Journal of Applied Physiology 2013;29(3):275-279
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the inhibition of Jumi (traditional Chinese medicine) extraction on the growth of human cervical cancer cell line HeLa.
METHODSNude mouse model of human cervical cancer HeLa cell transplantation was established. The nude mice bearing cancer were randomly divided into control group and Jumi treated groups with different concentration (0.001, 0.002, 0.005, 0.01 mg/ml). The growth of cervical cancer cell in experimental mice were measured. Cultured HeLa cells were incubated in culture media with or without Jumi extract for 48 hours. Cell proliferation rate, cell apoptosis, caspase-3/7 and caspase-6 activity were determined by MTT colorimetric assay, flow cytometry analysis and spectrophotometric detection, respectively.
RESULTSWith the increase of the concentration of Jumi extract, tumor-bearing mice tumor inhibition rate gradually increased. The proliferation of cultured HeLa cells were significantly inhibited by Jumi extract in a dose-dependent manner. IC50 was 0.004 mg/ml. Apoptosis rates in the cells treated with Jumi extract were higher than those of the control group. Compared with the control group, except for lower Jumi treated group (0.001 mg/ml), caspase-3/7 and caspase-6 activity were significantly increased in the all Jumi treated groups.
CONCLUSIONJumi extract can inhibit the proliferation of human cervical cancer cell line HeLa in vitro in a dose-dependent manner and promote cell apoptosis through caspase-3, caspase-7 and caspase-6 pathway.