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Objective:The interaction between lobetyolin and bovine serumal bumin（bovine serum albumin，BSA）. Method:By the steady-state fluorescence analysis method，the molecular-docking，ultraviolet absorption spectrum and fluorescence quenching were used to calculate quenching constant and binding constant，the number of sites，the position，the force and the distance of lobetyolin-BSA system. In addition， the effect of metalionson quenching constant of the lobetyolin-BSA system was studied. Result:The quenching constant was 1.25×104 L·mol-1（37 ℃），the binding constant was 2.95×104 L·mol-1（37 ℃），and the number of sites was 1 and bound with site 1 in ⅡA of BSA， thermodynamic meters were ΔH=-19.374 kJ·mol-1，ΔS=23.1 J·mol-1·K-1， the interaction distance was 3.2 nm. Meta lions could accelerate the quenching. Conclusion:By the steady-state fluorescence technique，molecular-docking and ultraviolet absorption spectrum，the quenching mechanism of Lobetyolin-BSA is quiescent quenching，and the interactive force is electro static force. The Lobetyolin-BSA can be well combined. At the same time，it also shows that the molecular docking results are similar to the experimental results obtained by steady-state fluorescence analysis.
RESUMEN
Objective:To investigate the effect of Ru′ai Shuhou prescription （RSR） drug-containing serum on the proliferation and invasion ability of breast cancer cells MDA-MB-453 based on the biological axis of stromal cell-derived factor-1（SDF-1）/chemokine receptor 4 （CXCR4）. Method:A model of MDA-MB-453 cells with SDF-1-induced high expression of CXCR4 was established， and the rat drug-serum containing RSR and blank rat serum were prepared respectively. The cells were divided into fetal bovine serum control group （Blank）， blank rat serum group， SDF-1+blank rat serum group， SDF-1+RSR group， AMD3100+ SDF-1+blank rat serum group， and AMD3100+ SDF-1+RSR group. After intervention for 48 h， cell proliferation was detected by cell counting kit-8 （CCK-8） assay， cell invasion ability was detected by transwell assay， and mRNA and protein expressions of CXCR4， matrix metalloproteinase-2 （MMP-2） and MMP-9 were detected by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot， respectively. Result:As compared with the blank serum group， the proliferation of MDA-MB-453 cells was promoted and expression of CXCR4 mRNA was increased significantly when SDF-1 was 100 μg·L-1 （P<0.05）. As compared with SDF-1+blank rat serum group， RSR inhibited the proliferation and invasion of MDA-MB-453 cells induced by SDF-1， and at the same time， down-regulated the mRNA and protein expressions of CXCR4， MMP-2 and MMP-9 （P<0.05）. After pre-treatment with AMD3100 for 24 h， the inhibitory effect of RSR to cell proliferation was significantly increased （P<0.05）， and meanwhile， the decreases in mRNA and protein expression of CXCR4， MMP-2 and MMP-9 were more obvious， with statistically significant differences （P<0.05）. Conclusion:Through SDF-1/CXCR4 biological axis， RSR could down-regulate the expression of MMP-2 and MMP-9， reduce the degradation of extracellular matrix （ECM）， and then inhibit the metastasis of MDA-MB-453 cells. In addition， it has a synergistic effect with CXCR4 inhibitor AMD3100.
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<p><b>OBJECTIVE</b>To observe the anti-tumor recurrent and metastatic efficacy of Ru'ai Shuhou Recipe (RSR) on HER2 positive breast cancer, to evaluate the effects of RSR on the expressions of matrix metalloproteinases (MMPs) and the tissue inhibitor of metalloproteinases (TIMPs) in the recurrence and metastasis of HER2 positive breast cancer, thus revealing its anti-tumor recurrent and metastatic mechanisms.</p><p><b>METHODS</b>Selected were 30-week-old HER2/neu transgenic spontaneous breast cancer mice FVB/neu. The primary tumor resection was carried out. After surgery they were randomly divided into the blank control group, the RSR group, the Herceptin group, and the combination group (RSR + Herceptin group). The treatment lasted for 4 months. The inhibition rate of the recurrent tumor volume and the inhibition rate of the lung metastasis were evaluated. The expressions of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase (TIMP-1), and TIMP-2 in the recurrent tumor tissue were detected using Western blot.</p><p><b>RESULTS</b>By the end of the treatment the average recurrent tumor volume was 11.11 +/- 8.71 cm3 in the blank control group and 5.56 +/- 5.55 cm3 of the RSR group, showing statistical difference between the two groups (P = 0.037). The average lung metastatic nodule was 16 in the blank control group and 10 in the RSR group. The inhibition rate of lung metastasis was 37. 85% in the RSR group, but with no statistical significance. The expression level of activated MMP-2 in the RSR group was down-regulated when compared with the blank control group, the Herceptin group, and the combination group (P < 0.05). The expression of MMP-9 of the RSR group, the Herceptin group, and the combination group was significantly down-regulated when compared with the blank control group (P < 0.05). The expression of MMP-9 of the RSR group and the combination group was further down-regulated when compared with the Herceptin group (P < 0.05). The expressions of both TIMP-1 and TIMP-2 of the RSR group, the Herceptin group, and the combination group were all up-regulated when compared with the blank control group (P < 0.05). The increased expression of TIMP-1 was more significantly in the RSR group and the combination group when compared with the Herceptin group (P < 0.05). It was higher in the combination group than in the RSR group (P < 0.05).</p><p><b>CONCLUSIONS</b>RSR could inhibit the tumor recurrence of FVB/neu mice. It could reduce the degradation of extracellular matrix and increase the protective effects of extracellular matrix. It might achieve its anti-tumor effect through effecting the invasive and metastatic capabilities of breast tumor cells.</p>