Low-dose aspirin induced autophagy comprises its inhibitory effect on HepG2 cells
10.19405/j.cnki.issn1000-1492.2018.03.009
- VernacularTitle:低剂量阿司匹林诱导产生的自噬减弱其对人肝癌HepG2细胞系的抑制作用
- Author:
Siya ZHU
1
;
Menglin WANG
;
Juan JIN
Author Information
1. 安徽医科大学基础医学院药理教研室
- Keywords:
aspirin;
human hepatocellular carcinoma HepG2 cells;
autophagy;
autophagy inhibitors
- From:
Acta Universitatis Medicinalis Anhui
2018;53(3):373-377
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the inhibitory effect of aspirin on proliferation of human hepatocellular carcinoma HepG2 cell line and its possible mechanismt. Methods MTT assay and plate cloning experiments was used to detect proliferation of human hepatoma HepG2 cells. Effects of aspirin on autophagosomes in HepG2 cells were detected by acridine orange fluorescence staining. The expression of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) protein in human hepatocellular carcinoma HepG2 cells was detected by Western blot. Results 10 mmol/L concentration of aspirin could inhibit the proliferation of HepG2 cells, but increase the number of autophagosomes of HepG2 cells, increase AMPK expression, decrease mTOR expression. After combination treatemnt with 40 μmol/L autophagy inhibitor chloroquine (CQ), CQ could enhance the inhibitory effect of 10 mmol/L aspirin on proliferation of human hepatoma HepG2 cells. Conclusion Combination treatment with autophagy inhibitor CQ attenuates 10 mmol/L aspirin-induced autophagy thus enhance its anti-HepG2 effect.
