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[Effects of shikonin on the proliferation and apoptosis of HL-60 cells].

Zhilu Chen, Qizhou Dai, Yong Wang

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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.

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What this paper is about

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.

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Available 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.

Key concepts: Apoptosis, Annexin, Cell growth, Pi, Molecular biology, Acute promyelocytic leukemia, MTT assay, Chemistry

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[Effects of shikonin on the proliferation and apoptosis of HL-60 cells]. — Research Paper | ScholarLens