ABSTRACT
BACKGROUND: Increasing studies have shown that solid lipid nanoparticles made from traditional Chinese medicine can inhibit cancer cell proliferation and induce cell apoptosis. OBJECTIVE: To investigate the mechanisms of oridonin solid lipid nanoparticles (ORI-SLN) by the regulation of Wnt/β-catenin signaling pathway on the proliferation and apoptosis of esophageal cancer cells. METHODS: After 0, 2.5, 5, 10, 20 μmol/L ORI-SLN treated human esophageal cancer cell lines Eca-109 for 24, 48, 72 hours, the cell inhibition rate was detected by cell counting kit-8, and the half maximal inhibitory concentration (IC50) was calculated. After 0, 14 μmol/L ORI-SLN treated Eca-109 cells for 48 hours, the cell apoptosis was detected by flow cytometry. The expression of Cleaved caspase3, β-catenin, C-myc, Cyclin D1 proteins was detected by western blot assay. Wnt/β-catenin signaling pathway activator LiCl and LiCl+ORI-SLN were used to treat Eca-109 cells for 48 hours, and then the relevant indicators were reexamined. Eca-109 cells without any treatment were used as controls. RESULTS AND CONCLUSION: The cell inhibition rate of Eca-109 cells treated with different concentrations of ORI-SLN for 24, 48 and 72 hours was significantly higher than that at 0 hour, and the cell inhibition rate was found to increase with the prolongation of time and the increase of the concentration (P < 0.01). 14 μmol/L ORI-SLN was confirmed to result in the higher cell apoptosis and Cleaved caspase3 expression compared with the 0 μmol/L group, while the expression of β-catenin, C-myc, Cyclin D1 proteins were significantly lower than the 0 μmol/L group (P < 0.01). Cell inhibition rate, apoptosis rate and Cleaved caspase3 protein expression in the activator group and ORI-SLN+activator group were significantly higher than those in the control group, and the expression of β-catenin, C-myc, Cyclin D1 protein was significantly lower than those in the control group (P < 0.01). The cell inhibition rate, apoptosis rate and expression of Cleaved caspase3 in ORI-SLN+activator group was significantly lower than those in the activator group, and the β-catenin, C-myc, Cyclin D1 protein expression was significantly higher than that in the activator group (P < 0.01). To conclude, ORI-SLNs can inhibit the proliferation and apoptosis of human esophageal carcinoma cell line Eca-109, and its mechanism is related to the regulation of Wnt/β-catenin signaling pathway.