RESUMEN
This study was aimed to establish an HPLC method for the content determination ofepimedin A, epimedinB,epimedinC,epimedium glycoside,baohuosideI in epimedium flavonoids capsule. The elusion was performed on an Eclipse Plus C18column (250 mm× 4.6 mm, 5μm). The mobile phase was composed of acetonitrile and water with a gradient elution. The flow rate was set at 1 mL·min-1. The detection wave length was set at 270 nm. The column temperature was 25℃. The results showed that the linear ranges of epimedin A,epimedinB,epimedinC,epimedium glycoside,baohuosideI were 3.10-62.00μg·mL-1, 5.70-114.00μg·mL-1, 9.14-182.80μg·mL-1, 15.20-304.00μg·mL-1, and 1.56-31.20μg·mL-1, respectively. The correlation coefficientr was more than 0.999 3. The average recoveries were 101.06% (RSD = 1.05%,n = 6), 100.78% (RSD = 1.08%,n = 6), 99.17% (RSD = 1.14%,n = 6), 100.23% (RSD = 0.68%,n = 6), and 99.09% (RSD = 1.30%,n = 6), respectively. This experiment was precise, reproducible and stable. It was concluded that the method was simple and accurate, which provided a certain reference value for the multi-component assaying of epimedium flavonoids capsule.
RESUMEN
Objective: To study the effect of baohuoside-I extracted from Periplocae Cortex on proliferation and Wnt/β-catenin signaling pathway of human esophageal carcinoma cell Eca-109. Methods: The expressions of β-catenin, Cyclin D1, and Survivin protein in Eca-109 cells were measured with flow cytometry (FCM). The expressions of β-catenin, Cyclin D1, and Survivin mRNA were detected by RT-PCR. Results: After treatment with 25 and 50 μg/mL of baohuoside-I for 48 h, the expression levels of β-catenin, Cyclin D1, Survivin mRNA, and protein were decreased significantly (P<0.01), but with 12.5 μg/ML of baohuoside-I the expression level was not decreased significantly compared with the control group. Conclusion: Baohuoside-I from Periplocae Cortex could inhibit the proliferation of Eca-109 cells. This effect associais with down-regulation expression of β-catenin, Cyclin D1, Survivin, and their proteins, which affects on the Wnt/β-catenin signaling pathway.