AIM:To investigate the role of autophagy in the antiapoptotic effect of augmenter of liver regeneration(ALR).METHODS:Autophagy was induced through serum deprivation.An ALR-expressing plasmid was transfected into HepG2 cells,and autophagic flux was determined using fluorescence microscopy,electron microscopy,Western blot and quantitative polymerase chain reaction(q PCR) assays.After ALR-expressing plasmid transfection,an autophagy inhibitor [3-methyladenine(3-MA)] was added to HepG2 cells,and apoptosis was observed using fluorescence microscopy and flow cytometry.RESULTS:Autophagy was activated in HepG2 cells,peaking at 24 h after serum deprivation.Microtubuleassociated protein light chain three-II levels were higher in HepG2 cells treated with ALR than in control cells,fluorescence microscopy,electron microscopy and q PCR studies showed the similar trend,and p62 levels showed the opposite trend,which indicated that ALR may play an important role in increasing autophagy flux.The numbers of apoptotic cells were substantially higher in HepG2 cells treated with both ALR and 3-MA than in cells treated with ALR alone.Therefore,the protective effect of ALR was significantly attenuated or abolished when autophagy was inhibited,indicating that the anti-apoptotic effect of ALR may be related to autophagy.CONCLUSION:ALR protects cells from apoptosis partly through increased autophagy in HepG2 cells and may be valuable as a new therapeutic treatment for liver disease. AIM: To investigate the role of autophagy in the antiapoptotic effect of augmenter of liver regeneration (ALR). METHODS: Autophagy was induced through serum deprivation. An ALR-expressing plasmid was transfected into HepG2 cells, and autophagic flux was determined using fluorescence microscopy, electron microscopy, Western blot and quantitative polymerase chain reaction (q PCR) assays. After ALR-expressing plasmid transfection, an autophagy inhibitor [3-methyladenine (3-MA)] was added to HepG2 cells, and apoptosis was observed using fluorescence microscopy and Flow cytometry .RESULTS: Autophagy was activated in HepG2 cells, peaking at 24 h after serum deprivation. Microtubuleassociated protein light chain three-II levels were higher in HepG2 cells treated with ALR than in control cells, fluorescence microscopy, electron microscopy and q PCR studies showed the similar trend, and p62 levels showed the opposite trend, which indicates that ALR may play an important role in increasing autophagy flux. The numbers of apoptotic cells were substantially higher in HepG2 cells treated with both ALR and 3-MA than in cells treated with ALR alone. Beforefore the protective effect of ALR was significantly attenuated or abolished when autophagy was inhibited, indicating that the anti-apoptotic effect of ALR may be related to autophagy. CONCLUSION: ALR protects cells from apoptosis partly through increased autophagy in HepG2 cells and may be valuable as a new therapeutic treatment for liver disease.