CGI-58 resists 5-FU induced macrophage apoptosis in vitro

郝丽君; 陈玉娟; 张璇; 梁后杰; 缪洪明; 阮志华

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CGI-58 resists 5-FU induced macrophage apoptosis in vitro

更新时间：2026-01-09

- CGI-58 resists 5-FU induced macrophage apoptosis in vitro
- Journal of Army Medical University Vol. 38, Issue 4, Pages: 367-373(2016)
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  CLC： R329.24;R965;R979.1
- Published：2016
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郝丽君,陈玉娟,张璇,梁后杰,缪洪明,阮志华.CGI-58抵抗5-FU诱导的巨噬细胞凋亡[J].陆军军医大学学报(原第三军医大学学报),2016,38(04):367-373.

　Hao Lijun,Chen Yujuan,Zhang Xuan,Liang Houjie,Miao Hongming,Ruan Zhihua.CGI-58 resists 5-FU induced macrophage apoptosis in vitro[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(04):367-373.
郝丽君,陈玉娟,张璇,梁后杰,缪洪明,阮志华.CGI-58抵抗5-FU诱导的巨噬细胞凋亡[J].陆军军医大学学报(原第三军医大学学报),2016,38(04):367-373. DOI：

　Hao Lijun,Chen Yujuan,Zhang Xuan,Liang Houjie,Miao Hongming,Ruan Zhihua.CGI-58 resists 5-FU induced macrophage apoptosis in vitro[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(04):367-373. DOI：

摘要

目的观察CGI-58对5-FU诱导的巨噬细胞凋亡的影响，并探讨其作用及机制。方法用5-FU处理巨噬细胞（PLKO）与CGI-58敲低（knockdown）的巨噬细胞（CGI-58 KD）后分别用CCK-8法检测其细胞增殖能力；流式细胞术检测其细胞周期与凋亡；Western blot检测其凋亡蛋白（cleaved Caspase-3）的表达水平；Seahorse Assays检测其线粒体功能。结果 CCK-8检测发现CGI-58 KD+5-FU组细胞活力降低更明显（P0.01）；流式细胞术结果显示经5-FU处理后，CGI-58 KD组的细胞凋亡率明显高于PLKO组（P0.01），Western blot检测发现CGI-58 KD+5-FU组cleaved Caspase-3的表达水平明显高于PLKO+5-FU组（P0.01）；Seahorse Assays检测发现CGI-58 KD组其基础耗氧率OCR明显降低（P0.01），ATP生成减少（P0.05），ROS表达增加（P0.01）；抗氧化剂NAC处理可拮抗巨噬细胞CGI-58缺失诱导的ROS增加（P0.05）、5-FU杀伤作用(P0.05)及cleaved Caspase-3表达水平。结论 CGI-58缺失可增强5-FU对巨噬细胞的杀伤作用并损伤巨噬细胞的线粒体功能，其作用机制可能是通过增加ROS的产生来实现的。

Abstract

Objective To determine the effect of CGI-58 on 5-fluorouracil(5-FU) induced macrophage apoptosis

and investigate the underlying mechanism. Methods CCK-8 assay was used to detect the effect of 5-FU on the proliferation of primary macrophage (PLKO) and CGI-58 knockdown macrophage (CGI-58 KD). Flow cytometry was used to test the cell cycle and apoptosis of PLKO and CGI-58 KD which were induced by 5-FU. Western blotting was employed to detect apoptosis protein (cleaved Caspase-3) and expression levels of 5-FU induced PLKO and CGI-58 KD. Seahorse assay was applied to test the mitochondrial function of PLKO and CGI-58 KD. Results CCK-8 assay found that the cell vitality of CGI-58 KD+5-FU group was reduced significantly (P0.01). Flow cytometry results showed that after 5-FU induction

the apoptotic rate of CGI-58 KD group was significantly higher than that of PLKO group (P0.01). Western blotting showed that the expression level of cleaved Caspase-3 in CGI-58 KD+5-FU group was obviously higher than that in PLKO+5-FU group (P0.01). Seahorse assay detected that the oxygen consumption rate of CGI-58 KD group was significantly decreased (P0.01)

ATP generation was reduced (P0.05)

and ROS expression was increased (P0.01). Antioxidant N-acetyl-L-cysteine could antagonize ROS increase induced by CGI-58 deletion (P0.05)

5-FU killing effect (P0.05) and expression of cleaved Caspase-3. Conclusion CGI-58 deletion can strengthen the killing effect of 5-FU on macrophage and damage the mitochondrial function of macrophage through increasing ROS.

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郝丽君

陈玉娟

张璇

梁后杰

缪洪明

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