1,25-dihydroxyvitamin D<sub>3</sub> induced Hep-2 cells apoptosis through PI3K/AKT/Bcl-2 signaling pathway

Gui Mingcai; Li Bing; Qi Siguo; Zhou Changhua

doi:10.13406/j.cnki.cyxb.001071

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1,25-dihydroxyvitamin D₃ induced Hep-2 cells apoptosis through PI3K/AKT/Bcl-2 signaling pathway

更新时间：2024-01-17

- 1,25-dihydroxyvitamin D₃ induced Hep-2 cells apoptosis through PI3K/AKT/Bcl-2 signaling pathway
- Journal of Chongqing Medical University Vol. 42, Issue 11, Pages: 1422-1425(2017)
- 作者机构：
  
  1. 达州市中心医院耳鼻咽喉头颈外科
  2. 重庆医科大学附属第一医院耳鼻咽喉科
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.001071
  CLC： R739.65
- Published：2017，
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Gui Mingcai, Li Bing, Qi Siguo, et al. 1,25-dihydroxyvitamin D₃ induced Hep-2 cells apoptosis through PI3K/AKT/Bcl-2 signaling pathway. [J]. Journal of Chongqing Medical University 42(11):1422-1425(2017)
DOI：

Gui Mingcai, Li Bing, Qi Siguo, et al. 1,25-dihydroxyvitamin D₃ induced Hep-2 cells apoptosis through PI3K/AKT/Bcl-2 signaling pathway. [J]. Journal of Chongqing Medical University 42(11):1422-1425(2017) DOI： 10.13406/j.cnki.cyxb.001071.

摘要

目的:研究1

25-二羟维生素D3诱导人喉癌Hep-2细胞凋亡及其对PI3K/AKT/Bcl-2信号通路的影响。方法:用不同剂量(10-8、10-7、10-6 mol/L)1

25-二羟维生素D3处理Hep-2细胞24、48、72 h

四甲基偶氮唑蓝法(MTT)检测Hep-2细胞的增殖情况

计算抑制率。流式细胞术检测Hep-2细胞的凋亡率。Western blot检测用药前后细胞中PI3K、AKT及其磷酸化、Bax和Bcl-2蛋白的表达水平。结果:MTT结果显示

25-二羟维生素D3可以抑制Hep-2细胞增殖(P<0.05)

25-二羟维生素D3浓度为10-6 mol/L抑制率可达30.71%

在上述浓度内随着浓度增加和时间延长

抑制作用逐渐增强

呈时间-剂量依赖性。流式细胞术检测到10-8、10-7、10-6 mol/L 1

25-二羟维生素D3作用48 h后

Hep-2凋亡细胞比例显著增加

凋亡率分别为12.13%、14.05%、16.17%

高于空白对照组的6.82%(P<0.05)。Western blot检测结果显示1

25-二羟维生素D3处理48 h后

Hep-2细胞PI3K、AKT、p-AKT、Bcl-2蛋白表达降低

Bax蛋白表达升高(P<0.05)。结论:在一定浓度范围内

25-二羟维生素D3(10-6、10-7、10-8mol/L)能够抑制人喉癌Hep-2细胞增殖

呈时间-剂量依赖性

其抑制作用与诱导细胞凋亡有关;1

25-二羟维生素D3可通过影响PI3K/AKT/Bcl-2

从而诱导Hep-2细胞凋亡。

Abstract

Objective:To study 1

25-dihydroxyvitamin D

induced apoptosis in Hep-2 cells and its effect on PI3 K/AKT/Bcl-2 signaling pathway. Methods:Hep-2 cells were processed by different concentrations of 1

25-dihydroxyvitamin D

（10-8

10-7 and 10-6 mol/L）for 24

48 and 72 h. The Hep-2 cells proliferation and inhibition rate were detected and calculated by methyl thiazolyl tetrazolium（MTT）. Apoptosis rate of Hep-2 cells was detected by flow cytometry. The expression levels of PI3 K/AKT/Bcl-2 were analyzed by Western blot. Results:MTT results showed that 1

25-dihydroxyvitamin D

can inhibit the proliferation of Hep-2 cells（P

0.05）.1

25-dihydroxyvitamin D

concentration of 10-6 mol/L inhibition rate was up to 30.71%

in a time-and dose-dependent manner.Flow cytometry showed 1

25-dihydroxyvitamin D

with 10-8

10-7 and 10-6 mol/L significantly increased Hep-2 cell apoptosis rate after48 h;the apoptosis rates were 12.13%

14.05%

16.17% respectively

higher than 6.82% of the normal control group（P

0.05）. Western blot results showed that Bax protein expression increased and PI3 K/AKT/p-AKT/Bcl-2 protein expression decreased after 1

25-dihydroxyvitamin D

treatment for 48 h. Conclusion:A certain range of concentration of 1

25-dihydroxyvitamin D

（10-6

10-7 and10-8 mol/L）can inhibit proliferation of human laryngeal carcinoma Hep-2 Cells

in a time and dose dependent manner

probably through induced apoptosis. 1

25-dihydroxyvitamin D

can up-regulate Bax protein expression and down-regulate PI3 K/AKT/p-AKT/Bcl-2 protein expression to induce the apoptosis of Hep-2 cells.

关键词

125-二羟维生素D3喉癌Hep-2细胞PI3K/AKT/Bcl-2

Keywords

125-dihydroxyvitamin D3laryngeal carcinomaHep-2 cellsPI3K/AKT/Bcl-2

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重庆医科大学临床学院耳鼻咽喉科

⁰

1,25-dihydroxyvitamin D3 induced Hep-2 cells apoptosis through PI3K/AKT/Bcl-2 signaling pathway

DOI：10.13406/j.cnki.cyxb.001071

摘要

Abstract

关键词

Keywords

references

1,25-dihydroxyvitamin D₃ induced Hep-2 cells apoptosis through PI3K/AKT/Bcl-2 signaling pathway