OBJECTIVE： To explore the signaling pathway of α-momordicin inducing early apoptosis of hepatocyte L02 （called “the L02 cell” for short）. METHODS： α-momordicin was prepared and purified. Flow cytometry was used to detect the apoptotic rate of the L02 cell after treated with 0 （negative control）， 160 and 80 μg/mL of α-momordicin for 2-8 h. LRP1-siRNA cells were obtained by small interfering RNA （siRNA） silencing low density lipoprotein receptor-related protein 1 （LRP1）. The expression of proapoptotic protein p-JNK， p-Bad， Caspase-9， inhibitor of apoptosis protein p-p53， p-Akt，p-Bcl-2 and active Caspase-8 in the L02 cell （normal group） and LRP1-siRNA （silence group） after treated with α-momordicin for 0， 0.25， 0.5， 1， 2 h were determined by liquid biochip analysis in c-Jun N-terminal kinase （JNK） signaling pathway. Effects of α-momordicin on JNK signaling pathway were analyzed. RESULTS： α-momordicin could be prepared and purified （purity＞97％）. Compared with negative control group， 160 μg/mL α-momordicin could significantly induced early apoptosis of the cell after treated for 8 h （P＜0.05）； early apoptosis of the cell induced by 80 μg/mL α-momordicin was not obvious （P＞0.05）. Compared with 0 h， the expression of p-JNK， p-Bad and Caspase-9 were increased significantly and even reached the peak value 0.25 h after medication （P＜0.05）， while the expression of p-p53， p-Akt， p-Bcl-2 and Caspase-8 had no change. Compared with normal group， the expression of p-JNK， p-Bad and Caspase-9 of silence group were decreased significantly at different time points （P＜0.05）. CONCLUSIONS： α-momordicin can induce the apoptosis of hepatocytes via LRP1 receptor mediated JNK signaling pathway， and will provide the reference for its hepatotoxicity.