Abstract | OBJECTIVE: To explore the mechanism of shikonin for inducing the apoptosis of human promyelocytic leukemia cell HL-60. METHODS: The effects of shikonin on the HL-60 cell proliferation were detected using MTT. The apoptosis rate was analyzed by Annexin-V/PI double staining. The expression level of the bcl-2 gene was detected using semi-quantitative reverse transcriptase PCR (RT-PCR), thus analyzing the correlation between the bcl-2 expression level and the apoptosis of HL-60. RESULTS:
Shikonin could inhibit the proliferation of HL-60 cells with the concentration range of 1-8 microg/mL in a time- and concentration-dependent manner. Two microg/mL shikonin could induce the apoptosis of HL-60 cells in a time-dependent manner. The expression level of bcl-2 was obviously down-regulated at 2 microg/mL shikonin. CONCLUSIONS:
Shikonin could induce the apoptosis of HL-60 cells. Its mechanism was correlated with down-regulation of the expression level of bcl-2.
|
Authors | Zhi-Lu Chen, Qi-Zhou Dai, Yong Wang |
Journal | Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine
(Zhongguo Zhong Xi Yi Jie He Za Zhi)
Vol. 32
Issue 2
Pg. 239-43
(Feb 2012)
ISSN: 1003-5370 [Print] China |
PMID | 22574601
(Publication Type: English Abstract, Journal Article, Research Support, U.S. Gov't, Non-P.H.S.)
|
Chemical References |
- Naphthoquinones
- Proto-Oncogene Proteins c-bcl-2
- shikonin
|
Topics |
- Apoptosis
(drug effects)
- Cell Proliferation
(drug effects)
- HL-60 Cells
- Humans
- Naphthoquinones
(pharmacology)
- Proto-Oncogene Proteins c-bcl-2
(metabolism)
|