细胞黏附对干扰素、5-氟尿嘧啶诱导细胞凋亡的影响

胡文艳; 高建; 李璇; 田绿; 彭湃澜; 王峰; 高昌益; 任红; 唐开福

您当前的位置：

首页 >

文章列表页 >

细胞黏附对干扰素、5-氟尿嘧啶诱导细胞凋亡的影响

论著 | 更新时间：2026-01-09

- 细胞黏附对干扰素、5-氟尿嘧啶诱导细胞凋亡的影响
- Effects of cell adhesion on interferon and 5-fluorouracil induced cell apoptosis in vitro
- 陆军军医大学学报 2011年33卷第2期页码：124-127
- 作者机构：
- 作者简介：
- 基金信息：
- DOI：
  中图分类号： R329.2;R394.2;R73-354
- 纸质出版：2011
- 稿件说明：
移动端阅览
胡文艳,高建,李璇,田绿,彭湃澜,王峰,高昌益,任红,唐开福.细胞黏附对干扰素、5-氟尿嘧啶诱导细胞凋亡的影响[J].陆军军医大学学报(原第三军医大学学报),2011,33(02):124-127.

　Hu Wenyan,Gao Jian,Li Xuan,Tian Lu,Peng Pailan,Wang Feng,Gao Changyi,Ren Hong,Tang Kaifu.Effects of cell adhesion on interferon and 5-fluorouracil induced cell apoptosis in vitro[J].J Amry Med Univ (J Third Mil Med Univ),2011,33(02):124-127.
胡文艳,高建,李璇,田绿,彭湃澜,王峰,高昌益,任红,唐开福.细胞黏附对干扰素、5-氟尿嘧啶诱导细胞凋亡的影响[J].陆军军医大学学报(原第三军医大学学报),2011,33(02):124-127. DOI：

　Hu Wenyan,Gao Jian,Li Xuan,Tian Lu,Peng Pailan,Wang Feng,Gao Changyi,Ren Hong,Tang Kaifu.Effects of cell adhesion on interferon and 5-fluorouracil induced cell apoptosis in vitro[J].J Amry Med Univ (J Third Mil Med Univ),2011,33(02):124-127. DOI：

摘要

目的探讨细胞黏附作用对干扰素、5-氟尿嘧啶（5-Fu）诱导细胞凋亡的影响。方法采用HepG

、HEK293细胞株，常规96孔板培养细胞，分为空白不加药（A组）、多聚赖氨酸包被预处理+贴壁后加药（B组）、贴壁后加药（C组）、未贴壁就加药（D组）、未贴壁就加药和Fn抗体（E组）。选用干扰素、5-Fu分别作用各组细胞，MTT法测定各组增殖抑制率和DNA Fragmentation ELISA测定凋亡率，Western blot检测干扰素诱导各组PKR蛋白水平的表达。结果经多聚赖氨酸包被预处理后，细胞对药物的敏感性减弱，MTT法显示抑制率:干扰素作用G

细胞，B、C组抑制率分别为(27.24±31.77)%、(39.04±14.88)%（P0.05）；5-Fu作用G

细胞，B、C组抑制率分别为(30.61±11.26)%、(32.94±20.93)%（P0.05）；干扰素作用293细胞，B、C组抑制率分别为(32.02±23.48)%、(46.22±25.20)%（P0.05）；5-Fu作用293细胞，B、C组抑制率分别为(14.07±21.91)%、(31.61±31.49)%（P0.05)。DNA Fragmentation ELISA示凋亡率：干扰素作用G

细胞，B、C组凋亡率分别为(0.425±0.038)、(0.535±0.039)（P0.05）；5-Fu作用G

细胞，B、C组凋亡率分别为(0.337±0.016)、（0.417±0.075)（P0.05）；干扰素作用293细胞，B、C组凋亡率分别为（0.394±0.033)、（0.499±0.018)（P0.05）；5-Fu作用293细胞，B、C组凋亡率分别为（0.406±0.024)、（0.504±0.069)（P0.05)。而阻断纤维黏连蛋白（Fn），细胞对药物的敏感性增强，MTT法显示抑制率:干扰素作用G

细胞，D、E组抑制率分别为（49.90±11.90)%、（66.86±24.66)%（P0.05）； 5-Fu作用G

细胞，D、E组抑制率分别为（45.96±21.27)%、（68.76±31.41)%（P0.05）；干扰素作用293细胞，D、E组抑制率分别为（58.98±32.96)%、（76.72±21.69)%（P0.05）；5-Fu作用293细胞，D、E组抑制率分别为（47.02±26.84)%、（62.60±29.79)%（P0.05)。DNA Fragmentation ELISA示凋亡率:干扰素作用G

细胞，D、E组凋亡率分别为（0.699±0.023)、（0.801±0.040)（P0.05）；5-Fu作用G

细胞，D、E组凋亡率分别为（0.581±0.023)、（0.721±0.027)（P0.05）；干扰素作用293细胞，D、E组凋亡率分别为（0.555±0.011)、（0.686±0.040)（P0.05）；5-Fu作用293细胞，D、E组凋亡率分别为（0.590±0.062)、（0.704±0.011)（P0.05)。干扰素诱导各组PKR蛋白表达水平中，空白对照组分别较其他组显著下调（P0.05），而B、C、D、E组间表达差异无显著性（P0.05）。结论干扰细胞-基质的黏附作用可以增强干扰素、5-Fu的敏感性，从而使细胞增殖受抑，凋亡增加；干扰素可增强PKR磷酸化水平，但并不受黏附作用的影响。

Abstract

Objective To investigate the effects of cell adhesion on interferon (IFN) and 5-fluorouracil (FU) induced cell apoptosis. Methods HepG

and HEK293 cells were classified into the 5 groups. Cells in group A were seeded into blank plates and not treated. Cells in group B were seeded into polylysine precoated plates followed by 5-Fu (250 μg/ml 4.2 μl) or IFN (500 U/ml 1.7 μl) treatment in 6 h after seeding. Cells in group C were seeded into blank plates and treated with 5-Fu or IFN in 6 h after seeding. Cells in group D were seeded into blank plates and treated with 5-Fu or IFN immediately after seeding. Cells in group E were seeded into blank plates and treated with anti-fibronectin antibody (500 μg/ml

1 μl) immediately after seeding

and then treated with 5-Fu or IFN in 6 h after seeding. Cell proliferation was detected by MTT assay

and cell apoptosis was detected by DNA fragmentation ELISA assay. Western blotting was used to detected PKR content in IFN-induced groups. Results Polylysine precoating plates decreased the drug sensitivity of cells. MTT assay showed that IFN on HepG

cells

the proliferation of B and C groups was inhibited by (27.24±31.77)% and (39.04±14.88)% respectively (P0.05); 5-Fu on HepG

cells

the proliferation of B and C groups was inhibited by (30.61±11.26)% and (32.94±20.93)% respectively (P0.05); IFN on 293 cells

the proliferation of B and C groups was inhibited by (32.02±23.48)% and (46.22±25.20)% respectively (P0.05); 5-Fu on 293 cells

the proliferation of B and C groups was inhibited by (14.07±21.

91)% and (31.61±31.49)% respectively (P0.05). DNA fragmentation ELISA indicated IFN on HepG

cells

the apoptosis of B and C groups was (0.425±0.038) and (0.535±0.039) respectively (P0.05); 5-Fu on HepG

cells

the apoptosis of B and C groups was (0.337±0.016) and (0.417±0.075) respectively (P0.05); IFN on 293 cells

the apoptosis of B and C groups was (0.394±0.033) and (0.499±0.018) respectively (P0.05); 5-Fu on 293 cells

the apoptosis of B and C groups was (0.406±0.024) and (0.504±0.069) respectively (P0.05). However

blocking the antifibronectin antibody (Fn) enhanced the drug sensitivity to cells. MTT assay showed that IFN on HepG

cells

the proliferation of D and E groups was inhibited by (49.90±11.90)% and (66.86±24.66)% respectively (P0.05); 5-Fu on HepG

cells

the proliferation of D and E groups was inhibited by (45.96±21.27)% and (68.76±31.41)% respectively (P0.05); IFN on 293 cells

the proliferation of D and E groups was inhibited by (58.98±32.96)% and (76.72±21.69)% respectively (P0.05); 5-Fu on 293 cells

the proliferation of D and E groups was inhibited by (47.02±26.84)% and (62.60±29.79)% respectively (P0.05). DNA fragmentation ELISA indicated IFN on HepG

cells

the apoptosis of D and E groups was (0.699±0.023) and (0.801±0.040) respectively (P0.05); 5-Fu on HepG

cells

the proliferation of D and E groups was (0.581±0.023) and (0.721±0.027) respectively (P0.05); IFN on 293 cells

the proliferation of D and E groups was (0.555±0.011) and (0.686±0.040) respectively (P0.05); 5-Fu on 293 cells

the proliferation of D and E groups was (0.590±0.062) and (0.704±0.011) respectively (P0.05). Western blot analysis showed PKR was decreased in blank group compared with the other groups respectively (P0.05)

however

there was no significant difference among B

D and E groups (P0.05). Conclusion Repression of cell adhesion enhances the sensitivity of cells to IFN and 5-Fu treatment. IFN enhances the phosphorylation of PKR

but has n

o relationship with cell adhesion.

关键词

Keywords

references

浏览量

下载量

CSCD

文章被引用时，请邮件提醒。

提交

工具集

关联资源

静息期精原前体细胞Rb1基因敲除致精原干细胞特化异常机制初探

生物钟基因PER1调控口腔鳞癌细胞中BAX、BCL2和PCNA表达的昼夜节律

靶向抑制DNAJC1基因对多发性骨髓瘤细胞凋亡和增殖的影响

0.22太赫兹电磁辐射暴露致神经母细胞瘤Neuro-2a细胞损伤的非热效应研究