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.
ABSTRACT
Autophagy is the process of removing the lysosomal and use of degradation products,which can keep the balance of protein metabolism and maintain a stable cellular environment,thus autophagy is extensively involved in various pathophysiological processes.In recent years,although there has been some progress in the molecular and regulation mechanisms of autophagy,however,the research on autophagy and nervous system diseases has only just begun.Studies of rats with brain damage have shown that injection of autophagy inhibitors reduced extent of convulsions.Therefore we put forward scientific hypothesis that autophagy is associated with brain injury and signal transduction,and autophagy may aggravate brain damage by certain signaling pathways.This article outlines the new progresses of autophagy and autophagy inhibitors,and further explore its effects on the nervous system.