OBJECTIVE： To study the effect and its mechanism of carvedilol on leptin-induced activation and proliferation of LX2 human hepatic stellate cells （HSC-LX2）. METHODS： HSC-LX2 with logarithmic growth periods were divided into blank control group， leptin-stimulated group and carvedilol low-concentration， medium-concentration， high-concentration groups （5， 10， 20 μmol/L）. Except for the blank control group， other groups were added 0.1 g/L leptin and corresponding concentration of carvedilol. After 24 h， MTT method was used to detect the optical density （OD） value of cells and calculate the proliferation rate. Flow cytometry was used to detect the cell cycle and apoptosis. Real-time fluorescence quantitative polymerase chain reaction method was used to detect the α-smooth muscle actin （α-SMA）， matrix metalloproteinase inhibition factor 1 （TIMP-1）， leptin， leptin receptor mRNA expressions. Western blot method was used to detect phosphorylated Janus kinase 2 （p-JAK2）， phosphorylated signal transduction and transcriptional activator 3 （p-STAT3） protein expressions. RESULTS： Compared with blank control group， OD value of cell was increased in leptin-stimulated group； apoptotic rate was decreased； cells of G0/G1 were decreased； α-SMA， TIMP-1， leptin， leptin receptor mRNA expressions and p-JAK2， p-STAT3 protein expressions were increased （P＜0.05）. Compared with leptin-stimulated group， OD values of cells were decreased in carvedilol concentration groups； apoptotic rate was increased， and the cells were mainly blocked in G0/G1 phase； α-SMA， TIMP-1， leptin， leptin receptor mRNA expressions and p-JAK2， p-STAT3 protein expressions were decreased （P＜0.05） and was concentration-depended （P＜0.05）. CONCLUSIONS： Carvedilol can inhibit the activation and proliferation of leptin-induced HSC-LX2， promote its apoptosis. The mechanism may associate with down-regulating leptin， leptin receptor gene expression and blocking JAK2/STAT3 signal pathway activation by leptin in cells.