Excessive TGF-b1 facilitated overproduction of scar fibroblasts, while scar fibroblasts further secreted more MMP-1 to degrade collagen protein. LEO evidently decreased the Diperodon expression levels of MMP-1 and TGF-b1 mainly by induction of Lathyrol apoptosis in scar fibroblasts. Apoptotic cell death is mediated by molecular pathways that culminate in the activation of a family of cysteine proteases, known as the caspases, which orchestrate the dismantling and clearance of dying cells. There is considerable evidence demonstrating that activation of caspase-9 has significant relationships with scar fibroblast apoptosis. Caspase-3 activity has been described to be essential for drug-induced apoptosis, and caspase-9 is necessary for the process of apoptosis in scar fibroblasts. In the process of cell apoptosis, pro-caspase-9 is recruited to the ����apoptosome���� complex, while the recruitment causes caspase-9 cleavage and further activates downstream executioner caspases such as caspase-3. The activation of caspase-9 and -3 via the release of cytochrome c can induce apoptosis in scar fibroblasts in vivo. In order to further verify apoptosis in scar fibroblasts, we detected the mRNA expression levels of caspase-3 and caspase-9. After treatment with LEO for 28 days, the mRNA expression of caspase-3 and -9 increased markedly and dose-dependently compared with the control group, suggesting that LEO facilitated fibroblast apoptosis in scar tissue. In a previous study, we also found that EO significantly inhibited the growth of cultured HSFs, and induced cell apoptosis. Based on these findings, we deduce that LEO alleviates formed hypertrophic scars mainly through inhibition of HSF proliferation and induction of HSF apoptosis, as the abnormal biological behaviour of fibroblasts plays a central role in hypertrophic scar formation and development. Fibroblasts synthesize both type I and type III collagens, which are the main components of the ECM, and also excrete TGF-b1 and MMP-1, which regulate the synthesis and degradation of collagen. In conclusion, LEO alleviates produced hypertrophic scars in the rabbit ear model, mainly by inhibiting HSF proliferation and inducing HSF apoptosis, which further downregulates the mRNA expression of TGF-b1 and MMP-1, and upregulates degradation of collagen types I and III. LEO is potentially an effective cure for human hypertrophic scarring.