Tetrandrine induces retinoblastoma cells apoptosis via ROS induction and PI3K/Akt inhibition

张　静; 沈永青; 仇　炜

doi:10.3969/j.issn.1007-3969.2015.12.006

您当前的位置：

首页 >

文章列表页 >

Tetrandrine induces retinoblastoma cells apoptosis via ROS induction and PI3K/Akt inhibition

更新时间：2025-12-31

- Tetrandrine induces retinoblastoma cells apoptosis via ROS induction and PI3K/Akt inhibition
- China Oncology Vol. 25, Issue 12, Pages: 953-958(2015)
- 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
  3. 石家庄市鹿泉区人民医院外科,河北,石家庄,050020
  4. 首都医科大学附属北京友谊医院泌尿外科,北京,100050
- 作者简介：
- 基金信息：
- DOI：10.3969/j.issn.1007-3969.2015.12.006
  CLC：
- Published Online：03 February 2016，
  
  Published：03 February 2015
- 稿件说明：
移动端阅览
张　静,沈永青,仇　炜,等. 粉防己碱诱导人视网膜母细胞瘤细胞凋亡及其机制研究[J]. 中国癌症杂志, 2015, 25(12): 953-958.

张　静, 沈永青, 仇　炜. Tetrandrine induces retinoblastoma cells apoptosis via ROS induction and PI3K/Akt inhibition[J]. China Oncology, 2015, 25(12): 953-958.
张　静,沈永青,仇　炜,等. 粉防己碱诱导人视网膜母细胞瘤细胞凋亡及其机制研究[J]. 中国癌症杂志, 2015, 25(12): 953-958. DOI： 10.3969/j.issn.1007-3969.2015.12.006.

张　静, 沈永青, 仇　炜. Tetrandrine induces retinoblastoma cells apoptosis via ROS induction and PI3K/Akt inhibition[J]. China Oncology, 2015, 25(12): 953-958. DOI： 10.3969/j.issn.1007-3969.2015.12.006.

摘要

背景与目的：粉防己碱(tetrandrine，Tet)是一种天然化合物，其抗视网膜母细胞瘤作用尚不清楚。该研究拟检测Tet对人视网膜母细胞瘤细胞的抗肿瘤作用，并进一步阐明其作用机制。方法：采用CCK-8法检测Tet对视网膜母细胞瘤细胞活力的抑制作用；应用Annexin V/PI法检测细胞凋亡情况；在2’

7’-二氯荧光素二乙酸酯(2’

7’-dichlorofluorescin diacetate，DCFH-DA)染色后，采用流式细胞术检测细胞内反应性活性氧(reactive oxygen species，ROS)含量；采用蛋白［质］印迹法(Western blot)检测细胞Akt、p-Akt蛋白表达量。结果：Tet显著抑制视网膜母细胞瘤细胞活力，Tet浓度为4、8、10和20 μmol/L处理细胞24 h时，WERI-Rb-1细胞抑制率分别为5.7%、25.0%、55.1%和84.9%，Y79细胞抑制率分别为2.4%、2.9%、23.8%和54.2% (P0.01)；10 μmol/L Tet处理细胞12、24和48 h时，WERI-Rb-1细胞抑制率分别为6.0%、45.5%和74.7%，Y79细胞抑制率分别为2.9%、19.4%和43.3%(P0.01)。Tet诱导细胞凋亡，以10 μmol/L Tet处理细胞24和48 h时，WERI-Rb-1细胞凋亡率分别为(23.70±1.75)%和(34.83±3.15)%，Y79细胞凋亡率分别为(9.62±2.69)%和(14.97±1.50)%(P0.01)，凋亡抑制剂Z-VAD-FMK能够显著抑制Tet对视网膜母细胞瘤细胞的凋亡诱导作用(P0.05)。10 μmol/L Tet作用细胞6及12 h后，细胞的ROS产生量较对照组明显上升(P0.01)，N-乙酰基-L-半胱氨酸(N-acetyl-L-cysteine，NAC)能够抑制Tet诱导产生的ROS(P0.01)，NAC抑制ROS后，细胞的凋亡率较单独Tet作用组明显下降(P0.01)。Tet能够抑制视网膜母细胞瘤细胞PI3K/Akt信号通路。结论：Tet诱导视网膜母细胞瘤细胞凋亡，该作用机制与细胞内ROS升高、PI3K/Akt信号通路抑制有关。

Abstract

Background and purpose: Tetrandrine is a natural compound whose role in retinoblastoma remains unclear. This study investigated the effects of tetrandrine (Tet) on human retinoblastoma cells. Methods: CCK-8 assays were performed to analyze the effects of Tet on viability of retinoblastoma cells. The apoptosis rate was determined by Annexin V/PI assays. After staining with 2′

7′-dichlorofluorescin diacetate (DCFH-DA)

cellular reactive oxygen species (ROS) was measured by flow cytometry. Akt and p-Akt were detected by Western blot. Results: Tet inhibited cell viability of retinoblastoma cells. After treatment with Tet (4

10 and 20 μmol/L) for 24 h

cell viability inhibition rates of WERI-Rb-I were 5.7%

25.0%

55.1% and 84.9%

whereas inhibition rates of Y79 cells were 2.4%

2.9%

23.8% and 54.2% (P0.01). In cells treated with 10 μmol/L of Tet for 12

24 and 48 h

cell viability inhibition rates of WERI-Rb-I were 6.0%

45.5% and 74.7%

whereas inhibition rates of Y79 cells were 2.9%

19.4% and 43.3% (P0.01). Tet induced retinoblastoma cell apoptosis. After treatment with Tet (10 μmol/L) for 24 and 48 h

apoptosis rates of WERI-Rb-I were (23.70±1.75)% and (34.83±3.15)%

respectively

whereas apoptosis rates of Y79 cells were (9.62±2.69)% and (14.97±1.50)%

respectively (P0.01). Apoptosis inhibitor Z-VAD-FMK attenuated Tet-induced cell death (P0.05). ROS levels were indeed increased in cells treated with Tet (10 μmol/L) for 6 and 12 h (P0.01)

while N-Acetyl-L-cysteine (NAC) decreased Tet-induced ROS (P0.01). After ROS was inhibited by NAC

apoptosis rate was decreased compared with the control (P0.01). Further study indicated that Tet inhibited PI3K/Akt pathway in retinoblastoma cells. Conclusion: Tet induces cell apoptosis via increasing ROS synthesis and inhibiting PI3K/Akt pathway.

关键词

Keywords

references

Views

1841

下载量

CSCD

Alert me when the article has been cited

提交

Tools

Publicity Resources

Mechanistic study on PLK4 regulation of invasion, proliferation and apoptosis in oral squamous cell carcinoma

Different preventive effects of four cardioprotective agents on mice with adriamycin-induced cardiotoxicity

The influence ofPRUNE2 gene point mutation on proliferation, apoptosis, invasion and migration of prostate cancer DU145 cells

Effect of KLK8 on apoptosis of colorectal cancer cells by regulating EGF and its mechanism

Molecular mechanism of miR-19b-3p regulating apoptosis of medullary thyroid cancer cells by targetingMTUS1

Related Author

Huan QIN

Jie WANG

Jie YANG

Yingjie HUA

Huijuan QU

Honghai JI

Yifan CHEN

Yihui SHEN

Related Institution

Department of Stomatology, Affiliated Hospital of Shandong Second Medical University

Shouguang Stomatological Hospital

School of Stomatology, Shandong Second Medical University

Department of Cardiology, Zhongshan Hospital, Fudan University

Shanghai Institute of Cardiovascular Diseases

AI问答

⁰