OBJECTIVE： To study the effects of celastrol on the proliferation and apoptosis of human hepatoma HepG2 cells， and investigate its mechanism. METHODS： CCK-8 method was used to determine the cell activity 24， 48， 72 h after treated by 2， 5， 10 μmol/L celastrol， and the proliferation inhibition rate and half inhibitory concentration （IC50） were calculated； flow cytometry was conducted to detect the cell apoptosis rate and cycle change 24 h after treated by 2， 5， 10 μmol/L celastrol， and the DMSO was used as negative control； rhodamine 123 staining method was used to determine the mitochondrial membrane potential 48 h after treated by 2， 5， 10 μmol/L celastrol， and the DMSO was used as negative control； Western blot was adopted to detect the pro-apoptotic related genes Bax and B lymphoma 2 （Bcl-2） protein expressions 0， 12， 24， 36 h after treated by 5 μmol/L celastrol. RESULTS： 2， 5， 10 μmol/L celastrol can inhibit cell proliferation， IC50 was 5.834 μmol/L. 2， 5， 10 μmol/L celastrol can induce apoptosis； 5， 10 μmol/L celastrol can block cell in G0/G1， S phases， compared with negative control group， with significant differences （P＜0.05 or P＜0.01）， and the above effects all showing certain concentration-dependent manner. 5 μmol/L celastrol can increase Bax protein expression and decrease Bcl-2 protein expression after cultured for 12， 24， 36 h， showing certain time-dependent manner； compared with 0 h， there was significant difference （P＜0.05 or P＜0.01）. CONCLUSIONS： Celastrol can obviously inhibit the proliferation of human hepatoma HepG2 cells and induce their apoptosis， and the mechanism may be related with strengthening mitochondrial permeability and promoting the release of apoptosis-inducing factor.