Effects of beta-elemene on proliferation and apoptosis of human multiple myeloma cell RPMI-8226.
- Author:
Hao CHEN
1
;
Liang SHI
;
Zhi-Yong CHENG
;
Li YAO
;
Ying-Ying YANG
;
Ling PAN
Author Information
1. Department of Hematology, The Second Hospital, Hebei Medical University, Shijiazhuang 050000, Hebei Province, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Humans;
Multiple Myeloma;
metabolism;
pathology;
Proto-Oncogene Proteins c-bcl-2;
metabolism;
Sesquiterpenes;
pharmacology;
Transcription Factor RelA;
metabolism
- From:
Journal of Experimental Hematology
2010;18(2):368-371
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to investigate the effect of beta-elemene on proliferation and apoptosis of human multiple myeloma cell line RPMI-8226 and its mechanism. The effect of beta-elemene on the growth of human multiple myeloma cell line RPMI-8226 was detected by MTT. The effect of beta-elemene on the apoptosis of RPMI-8226 cells was determined by flow cytometry with Annexin-V/PI staining. The effects of beta-elemene on the expression of BCL-2, caspase-3, DR-4 and NF-kappaB P65 proteins were analyzed by Western blot. The results showed that the beta-elemene obviously inhibited the proliferation of RPMI-8226 cells in both time- and dose-dependent manners. Treatment with 10 - 80 micromol/L beta-elemene for 48 hours induced apoptosis of RPMI-8226 cells in a dose-dependent manner. The expression of caspase-3 and DR-4 proteins in RPMI-8226 cells treated with beta-elemene increased in a time-dependent manner, while expressions of BCL-2 and NF-kappaB P65 proteins decreased. It is concluded that the beta-elemene can inhibit the proliferation of RPMI-8226 cells by inducing the cell apoptosis. Activating the mitochondrial and death receptor pathways of apoptosis and inhibiting the anti-apoptosis pathway may involve in the beta-elemene-induced apoptosis.
