Objective:To observe the effect of autophagy on bisdemethoxycurcumin (BDMC)-induced apoptosis in hepatocellular carcinoma HepG2 cells. Method:Cells were treated with 24 mg·L-1 BDMC or BDMC + 5 mol·L-1 3-methyladenine (3-MA) for 24

48 h

and then the cell activity was detected by methye thiazolye telrazlium (MTT) assay. Cells were treated with 24 mg·L-1 of BDMC alone or combination with 5 mol·L-1 3-MA for 48 h

and then the morphologies were observed by Hoechst 33342 staining by using inverted fluorescence microscope. The apoptosis rate and the mitochondrial membrane potential (MMP) were assessed by Annexin V/propidium iodide (PI) staining and Rhodamine 123 (Rh123) staining respectively; the protein expression levels of Beclin-1

LC3

cleaved Caspase-3

B-cell lymphoma-2 (Bcl-2)

and Bcl-2 associated X protein (Bax) were evaluated by Western blot. Result:As compared with the blank control group

BDMC could inhibit the proliferation and induce apoptosis in HepG2 cells

decrease the MMP

decrease the protein expression levels of pro-Caspase-3

Bcl-2

LC3-Ⅰ(P<0.01)

and increase the protein expression levels of cleaved Caspase-3

Bax

Beclin-1

LC3-Ⅱ(P<0.01); 3-MA could enhance the effect of BDMC-induced HepG2 cell apoptosis

increased the apoptotic rates (P<0.01)

decreased the MMP (P<0.01)

lowered the protein expression levels of pro-Caspase-3

Bcl-2 (P<0.01) and increased the protein expression levels of Beclin-1

LC3

and cleaved Caspase-3 (P<0.01). Conclusion:BDMC could induce apoptosis via a mitochondria pathway in HepG2 cells

and could induce cells autophagy which could inhibit the cell apoptosis.