[厚朴酚诱导人非霍奇金淋巴瘤Raji细胞凋亡及其可能机制]

[Honokiol-induced apoptosis of human non-Hodgkin lymphoma Raji cells and its possible mechanism].

作者信息

Chen Wei, Lin Guan-wen, Zhang Qing

机构信息

Department of Hematology, Guangdong Second Provincial People's Hospital, Guangzhou 510317, China.

出版信息

Nan Fang Yi Ke Da Xue Xue Bao. 2011 Nov;31(11):1918-21.

PMID:22126780

Abstract

OBJECTIVE

To investigate the apoptosis-inducing effect of honokiol on human non-Hodgkin lymphoma Raji cells and the possible mechanism.

METHODS

Raji cells were treated with different concentrations of honokiol, and the proliferation of the cells was detected using MTT assay. Flow cytometry was employed to analyze the cell cycle changes and apoptosis of honokiol-treated cells. Caspase 8 activity in the cells was measured by caspase 8 kit, and RT-PCR was used to detect the expression of apoptosis-related genes Bcl-2, Bad, and Bax.

RESULTS

Honokiol significantly inhibited the growth of Raji cells in a time- and dose-dependent manner, with IC(50) concentration of 17.53, 12.61, and 7.4 µg/ml at 12, 24, 48 h, respectively. Flow cytometry revealed cell cycle arrest at G0/G1 phase following honokiol treatment. The apoptosis rates of Raji cells treated with 7.5 and 15 µg/ml honokiol were significantly higher than that of the control cells [(18.24∓2.53)%, (28.44∓2.48)% vs (4.84∓1.15)%, P<0.01]. Caspase 8 activity in Raji cells was significantly enhanced by honokiol (P<0.05). The mRNA expression of the apoptosis-promoting gene Bad was significantly increased following honokiol treatment (P<0.01), while the expressions of Bcl-2 and Bax remained unchanged.

CONCLUSION

Honokiol can induce apoptosis in Raji cells possibly in relation to enhancement of caspase 8 activity and Bad gene expression.

摘要

目的

探讨厚朴酚对人非霍奇金淋巴瘤Raji细胞的凋亡诱导作用及其可能机制。

方法

用不同浓度的厚朴酚处理Raji细胞，采用MTT法检测细胞增殖情况。运用流式细胞术分析厚朴酚处理后细胞周期的变化及凋亡情况。用caspase 8试剂盒检测细胞中caspase 8的活性，采用RT-PCR法检测凋亡相关基因Bcl-2、Bad和Bax的表达。

结果

厚朴酚能显著抑制Raji细胞的生长，呈时间和剂量依赖性，在12、24、48 h时的IC(50)浓度分别为17.53、12.61和7.4 μg/ml。流式细胞术显示厚朴酚处理后细胞周期阻滞于G0/G1期。用7.5和15 μg/ml厚朴酚处理的Raji细胞凋亡率显著高于对照细胞[(18.24±2.53)%，(28.44±2.48)% 对 (4.84±1.15)%，P<0.01]。厚朴酚可显著增强Raji细胞中caspase 8的活性(P<0.05)。厚朴酚处理后促凋亡基因Bad的mRNA表达显著增加(P<0.01)，而Bcl-2和Bax的表达未发生变化。