紫檀芪诱导人视网膜母细胞瘤WERI-Rb-1细胞的细胞凋亡及其机制研究

张　静; 沈永青; 智利彩

doi:10.3969/j.issn.1007-3969.2015.11.010

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紫檀芪诱导人视网膜母细胞瘤WERI-Rb-1细胞的细胞凋亡及其机制研究

更新时间：2025-12-31

- 紫檀芪诱导人视网膜母细胞瘤WERI-Rb-1细胞的细胞凋亡及其机制研究
- Pterostilbene induces retinoblastoma WERI-Rb-1 cell apoptosis via autophagy induction
- 中国癌症杂志 2015年25卷第11期页码：900-904
- 作者机构：
  
  1. 石家庄市第四医院产前诊断中心,河北,石家庄,050011
  2. 河北中医学院护理学院,河北,石家庄,050020
- 作者简介：
- 基金信息：
  
  河北省医学科学研究重点课题(ZD20140032)。
- DOI：10.3969/j.issn.1007-3969.2015.11.010
  中图分类号：
- 网络出版：2016-02-01，
  
  纸质出版：2015-02-01
- 稿件说明：
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张　静,沈永青,智利彩,等. 紫檀芪诱导人视网膜母细胞瘤WERI-Rb-1细胞的细胞凋亡及其机制研究[J]. 中国癌症杂志, 2015, 25(11): 900-904.

张　静, 沈永青, 智利彩. Pterostilbene induces retinoblastoma WERI-Rb-1 cell apoptosis via autophagy induction[J]. China Oncology, 2015, 25(11): 900-904.
张　静,沈永青,智利彩,等. 紫檀芪诱导人视网膜母细胞瘤WERI-Rb-1细胞的细胞凋亡及其机制研究[J]. 中国癌症杂志, 2015, 25(11): 900-904. DOI： 10.3969/j.issn.1007-3969.2015.11.010.

张　静, 沈永青, 智利彩. Pterostilbene induces retinoblastoma WERI-Rb-1 cell apoptosis via autophagy induction[J]. China Oncology, 2015, 25(11): 900-904. DOI： 10.3969/j.issn.1007-3969.2015.11.010.

摘要

背景与目的：紫檀芪是一种天然抗氧化剂，其抗视网膜母细胞瘤的效果仍不明确。拟探讨紫檀芪对人视网膜母细胞瘤WERI-Rb-1细胞的细胞增殖、细胞凋亡及细胞自噬的作用，并初步阐明其作用机制。方法：采用细胞计数试剂盒(cell counting kit-8，CCK-8)法测定细胞的增殖活力，Annexin V/PI流式细胞术检测细胞凋亡，吖啶橙染色观察细胞内自噬囊泡的变化，蛋白［质］印迹法(Western blot)检测LC3B及P62蛋白的表达。结果：紫檀芪显著抑制WERI-Rb-1细胞的增殖活力(P0.01)，以25、50和100 μmol/L的药物浓度作用细胞24 h时，细胞增殖活力分别为(93.02±0.47)%、(55.10±2.04)%和(30.33±1.45)%；50 μmol/L紫檀芪处理细胞12、24和48 h时，细胞增殖活力分别为(88.38±3.70)%、(53.37±1.17)%和(29.60±1.05)%。紫檀芪显著诱导细胞凋亡(P0.01)，对照组、24和48 h细胞的凋亡率分别为(4.08±0.79)%、(13.44±2.12)%和(23.49±2.01)%。紫檀芪能够激活WERI-Rb-1细胞发生细胞自噬，上调LC3蛋白的表达，下调P62蛋白的表达，增加细胞内自噬囊泡的数量(P0.01)。3-MA及Beclin1 siRNA抑制细胞自噬后能够部分逆转紫檀芪的抗肿瘤作用(P0.01)。3-MA抑制细胞自噬后，紫檀芪处理组的细胞凋亡率为(12.97±2.09)%，3-MA+紫檀芪组为(8.35±1.11)%。siRNA敲低Beclin1后，紫檀芪处理组和siRNA+紫檀芪组的细胞凋亡率分别为(13.80±2.19)%和(9.62±0.52)%。结论：紫檀芪可以显著抑制WERI-Rb-1细胞的细胞增殖并激活细胞自噬促进细胞凋亡。

Abstract

Background and purpose: Pterostilbene is a natural antioxidant

whose role in retinoblastoma remains unclear. The aim of this study is to probe the effects of pterostilbene on the proliferation

apoptosis and autophagy in retinoblastoma WERI-Rb-1 cell lines. Methods: Cell counting kit-8 (CCK-8) assays were used to analyze the effects of pterostilbene on the proliferation of WERI-Rb-1 cells. Apoptosis rate was determined by Annexin V/PI. Autophagic vacuoles were observed by acridine orange staining. LC3 and P62 protein expressions were determined using Western blot. Results: Pterostilbene significantly inhibited the proliferation of WERI-Rb-1 cells (P0.01). The cell viability were (93.02±0.47)%

(55.10±2.04)% and (30.33±1.45)% after WERI-Rb-1 cells were treated with 25

50 and 100 μmol/L pterostilbene for 24 h

and the cell viability were (88.38±3.70)%

(53.37±1.17)%

(29.60±1.05)% after WERI-Rb-1 cells were treated with 50 μmol/L pterostilbene for 12

24 and 48 h. Pterostilbene induced cell apoptosis (P0.01)

the apoptosis rates of control group

24 h treated group and 48 h treated group were (4.08±0.79)%

(13.44±2.12)% and (23.49±2.01)%. Pterostilbene induced autophagy of WERI-Rb-1 cells

increased LC3 expression

downregulated P62 expression and increased the number of autophagic vacuoles in WERI-Rb-1 cells (P0.01). 3-MA and Beclin1 were able to rescue pterostilbene-induced cell death (P0.01). After 3-MA was used to blunt autophagosome formation

the apoptosis rate markedly decreased in 3-MA+pterostilbene-treated cells compared with cells treated with pterostilbene alone [(12.97±2.09)% vs (8.35±1.11)%]

and after siRNA was used to knockdown Beclin1

the apoptosis rate had the same change [(13.80±2.19)% vs (9.62±0.52)%]. Conclusion: Pterostilbene can inhibit the proliferation of WERI-Rb-1 cells and induce cell apoptosis via autophagy activation.

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