Abstract: Objective To investigate the effect of lobaplatin （LBP） on proliferation and apoptosis of human hepatic cancer cell line HepG2 and possible mechanisms. Methods Logarithmic growth phase HepG2 cells were used for study. Different concentrations of LBP （0， 2.5， 5， 10， 20 μmol／L） treated HepG2 cells for 48 hours. General morphological changes were observed under an optical microscope. MTS assay was used to detect the relative viability of HepG2 cells， and IC50 （50％ inbibiting concentration） was calculated. Hoechst 33258 staining and flow cytometry based on Annexin V-PI double staining were used to measure the apoptosis of HepG2 cells. Western blotting assay was used to detect the expression changes of Bax， Bak， Bcl-2， Bcl-XL，Mcl-1， Survivin and PARP-1 protein. Results Cell morphological observation showed LBP treated HepG2 cells for 48 hours with the increase of drug concentration the HepG2 cell density decreased， the number of swelling cytoplasm and floating rounded cells increased significantly. Hoechst33258 staining to test the typical apoptotic cells with nuclear fragmentation or nuclear condensation showed that LBP induced apoptosis， in a dose-dependent manner. MTS assay indicated LBP greatly inhibited HepG2 cell growth in a dose- and time-dependent manner. The proliferation rates of HepG2 cells treated with 2.5, 5, 10, 20 μmol/L LBP for 48 h were （92.11±1.79）％， （65.87±1.78）％，（51.57±0.81）％ and （33.11±1.47）％. After LBP treatment HepG2 cell for 48 hours the value of IC50 was 13.28 μmol／L. The apoptotic rates of HepG2 cells treated with 2.5, 5, 10, 20 μmol/L LBP for 48 h were （11.64±0.85）%, （20.99±2.21）%, （33.02±2.30）% and （40.77±1.58）%. The difference was significant between LBP treat group and control group （P＜0.05）. Western blotting analysis showed that 2.5, 5, 10, 20 μmol/L LBP down-regulated Bcl-2 and Mcl-1 protein expression， whereas upregulated Bax， Bid and PARP-1 expression. Bcl-XL， Bak and Survivin protein expression was not changed. Conclusion LBP significantly exerts anti-cancer effects through inducing cell growth inhibition and apoptosis， the possible mechanism is related to the regulation of apoptosis related proteins including Bax， Bid， Bcl-2 and Mcl-1.