Résumé
【Objective】 To study the effect of Salidroside(Sal) on platelet activation and aggregation and the interaction between human platelets and MDA-MB-468 cells of breast cancer. 【Methods】 Human platelets were collected, platelet suspension was prepared, and platelets were treated with different concentrations of Sal. The effects of Sal on platelet activation and aggregation were detected by thromboelastogram(TEG) and flow cytometry. Breast cancer MDA-MB-468 cells were cultured in vitro, and human platelets were treated with different concentrations of Sal, and then activated by thrombin. The effects of Sal on the interaction between platelets and MDA-MB-468 cells were analyzed by adhesion test and scratch test. 【Results】 TEG detection: The ADP inhibition rate in the blank control group was (10.97±12.69)%, and the ADP inhibition rate in all Sal intervention groups was higher than that in the blank control group (P<0.05). The AA inhibition rate was (8.11±7.84)% in the control group and (25.96±15.18) % in the 5 μmol/L Sal intervention group, and the difference was statistically significant (P<0.05).Flow cytometry: The expression of CD62P on platelet surface in 40 and 60 μmol/L Sal groups was (56.5±0.17)% and (65.50±0.36)%, respectively, and the difference was statistically significant compared with the positive control group (76.53±0.49)% (P<0.05). The percentages of PAC-1 expression on platelet surface in 40 and 60 μmol/L Sal groups were (62.20±0.10)% and (58.47±0.15)%, and the difference was statistically significant compared with the positive control group (72.10±0.20) % (P<0.05). Adhesion experiment: Platelets can have adhesion with MDA-MB-468 cells, and activated platelets have stronger adhesion ability. The adhesion rate in the Sal group was significantly lower than that in the positive control group, and was negatively correlated with the concentration of Sal. Scratch test: The cell mobility at 24 h in the positive control group was (12.71±0.70)%, and the cell mobility in each Sal treatment group was (4.51±0.44)%, (3.85±0.11)%, (5.37±0.36)%, (4.15±0.13)% and (3.55±0.38)%, respectively, showing significant decrease compared with the positive control group(P<0.05). After 48 h of Sal treatment, the cell mobility of 10, 20, 40 and 60μmol/L Sal groups decreased, and there was a statistical difference compared with the positive control group(P<0.05). 【Conclusion】 Sal can inhibit the adhesion between activated platelets mediated by thrombin and MDA-MB-468 cells and the migration of MDA-MB-468 cells.
Résumé
@#Objective： ：To investigatetheeffectofsalidroside(SAL)onthephenotype of dendritic cells (DCs) and the antitumor ability of cytotoxic T lymphocytes (CTL). Methods： ：Lewis lung cancer cell line 3LL, wild type (WT) C57BL/6 mice and TLR4-/- C57BL/6 mice were chosen for this study. Mice bone marrow derived DC precursor cells were obtained to differentiate into immature DCs, which were harvested on the sixth day of culture. CD11c+ DCs were obtained by magnetic beads screening, and further divided into PBS group, SAL group and lipopolysaccharide (LPS) group.After being cultured for 48 h, the effects of SAL on surface molecules and phagocytosis of DCs as well as the efffect of TLR4 pathway on the killing effect of T cells were detected by Fow cytometry. Results： ： Compared with PBS group, expressions of DC surface molecules CD80, CD86 and MHC Ⅱ significantly increased (all P<0.05), phagocytosis significantly decreased (P<0.05), and TLR4 expression level significantly increased (P<0.01) in SAL group; Compared with WT group, after being treated with SAL or LPS, the expressions of DC surface molecules CD80, CD86 and MHC Ⅱ decreased significantly in TLR4-/- group (all P<0.05); ComparedwithPBSgroup,theactivatedCTLinSALgroupexhibited a significantly elevated killing effect against lung cancer 3LLcells (P<0.05). Conclusion：SAL can induce DC maturation by regulating TLR4, thus improving the killing ability of T cells.