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Objective To analyze the main active components and potential molecular mechanism of Sophora flavescens against breast cancer based on network pharmacology and molecular docking. Methods The chemical constituents were collected and screened by TCMSP, ETCM database and literature review. The targets of active ingredients were predicted by Swiss Target Prediction database. Breast cancer-related targets were collected by GeneCards, TTD, Drugbank and OMIM. The anti-breast cancer targets of Sophora flavescens were screened by Venny 2.1.0 software. Cytoscape software was used to construct the network diagram of Sophora flavescens-key active ingredients-targets. STRING database was used to analyze the common targets, and PPI network diagram was constructed. GO function enrichment analysis and KEGG pathway enrichment analysis of key target proteins were performed by DAVID database and Hiplot online platform. Schrodinger software was used to calculate the molecular docking between the active ingredients and targets. Molecular biological methods were used to verify the key targets. Results A total of 36 active components with clear structures were screened from Sophora flavescens. 70 anti-breast cancer targets of Sophora flavescens were screened out. 12 core targets including EGFR, AKT1, ESR1, SRC, CYP19A1, AR and ABCB1 participate in endocrine resistance, EGFR tyrosine kinase inhibitors and estrogen signaling pathways in breast cancer. Moreover, the docking score between the core component and the key target AR is the highest. In vitro experiments showed that the extract of Sophora flavescens can inhibit the proliferation of breast cancer cells, induce cell apoptosis and up-regulate AR protein expression. Conclusion It was revealed that Sophora flavescens plays an anti-breast cancer role by regulating complex biological processes through multiple components acting on multiple targets and signaling pathways. The upregulation of AR protein by Sophora flavescens may become a new therapeutic strategy for the treatment of breast cancer.
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Bone is the most common metastatic site of breast cancer . And breast cancer metastasis to bone can lead to osteoporosis , hypercalcemia , spinal cord compression and pathological fracture , which seriously impact the patientsˊ quality of life and survival . Chinese herbs have a potential advantage in the treatment of breast cancer metastasis to bone. In recent ten years, a number of studies showed that Chinese medicine monomers, traditional Chinese medicine (TCM) extracts, and Chinese herbal compound prescriptions played a role in in-hibiting breast cancer cell proliferation , invading and relieving the bone destruction and bone pain by different molecular mechanisms .
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To investigate the effects of platycodin D in combination with different active ingredients of Chinese herbs under different therapeutic principles on proliferation and invasion of 4T1 and MDA-MB-231 breast cancer cell lines.
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To explore the inhibitory effects and to investigate the mechanisms of combined treatment of osthole, psoralen with aconitine on human breast cancer cell line MDA-MB-231BO.
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Objective: To explore the effects of different proportions of Fructus Cnidii (Shechuangzi) and Psoralea corylifolia (Buguzhi) on highly metastatic human breast cancer cell line MDA-MB-231BO and bone marrow stromal cell line ST-2 in vitro. Methods: Thirty-six female SD rats were randomly divided into 6 groups to prepare the drug-medicated sera by administering with different proportions of Fructus Cnidii and Psoralea corylifolia, including 4:0 group, 3:1 group, 1:1 group, 1:3 group, 0:4 group and control group. MDA-MB-231BO cells and ST-2 cells were cultured in Dulbecco's modified Eagle's medium containing drug-medicated serum. Inhibition rates of MDA-MB-231BO cells and ST-2 cells were measured by methyl thiazolyl tetrazolium (MTT) method; migration ability of MDA-MB-231BO cells was tested by a cell migration experiment; alkaline phosphatase activity (ALP) of ST-2 cells was measured by using 4-nitrophenyl phosphate disodium salt, and mineralized nodule formation of ST-2 cells was measured by alizarin red staining. Results: Sera contaning different proportions of Fructus Cnidii and Psoralea corylifolia inhibited the migration activity of MDA-MB-231BO cells as compared with the blank serum, and serum contaning Fructus Cnidii and Psoralea Corylifolia at proportion of 1:1 had the best function (P<0.01). Fructus Cnidii and Psoralea corylifolia at ratio of 1:1 also enhanced the ALP activity of ST2 cells (P<0.05) and increased the number of mineralized nodules of ST2 cells (P<0.01). Conclusion: Kidney-warming recipe of Fructus Cnidii and Psoralea corylifolia can inhibit proliferation and migration of MDA-MB-231BO cells and increase the activity of ST-2 cells.
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Objective: To observe the effects of Guanxinkang injection, a compound traditional Chinese herbal medicine, on ATP-sensitive potassium (K(ATP)) channel subunits in ischemic myocardial cells of rats, and to explore the mechanism of Guanxinkang in protecting myocardial ischemic reperfusion injuries. Methods: Forty-eight Wistar rats were randomly divided into normal group, untreated group, glibenclamide group, pinacidil group, Guanxinkang group and Guanxinkang plus glibenclamide group. The ventricular myocytes were prepared from hearts of normal rats by enzymatic dissociation method. The ischemic ventricular myocytes underwent perfusion with normal Tyrode solution for 10 min, then stopping perfusion 30 min, and followed by 45 min of reperfusion. The glibenclamide, pinacidil and Guanxinkang were added into ventricular myocytes solution directly. Then the solutions were placed at 4 degrees centigrade. After 24-hour freezing at -80 degrees centigrade, mRNA and protein expressions of KATP subunits Kir6.1, Kir6.2, SUR2A and SUR2B were measured by real-time quantitative polymerase chain reaction and Western blotting respectively. Results: In normal rat myocardial cells, there were SUR2A, Kir6.1, and Kir6.2 protein and gene expressions but no expression of SUR2B protein. In the untreated group, all subunit mRNA and protein expressions of KATP increased to some extent as compared with the normal group. Pinacidil, a potassium channel opener, significantly increased mRNA and protein expressions of KATP subunits, while the blocker glibenclamide had a reverse effect. Meanwhile, Guanxinkang injection significantly increased mRNA and protein expressions of K(ATP) subunits but with no significant difference as compared with pinacidil. Conclusion: Guanxinkang injection can obviously enhance the open of KATP channel and thus play a role in cardiovascular protection.
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AIM To assess antidiabetic and insulin sensitizing effect of a novel thiazolidinedione,neoglitazone, in different animal models of type 2 diabetes. METHODS Neoglitazone combined with low-dose insulin(0.2U·d-1 per mouse,sc)were given in streptozotiocin (STZ)-induced diabetic mice for 7 d to inspect its insulin-sensitive improvement. The antidiabetic effect of chronic oral treatment (8 wk) with neoglitazone on spontaneous diabetes mice (DB/DB mice) was examined. The levels of blood glucose were measured by a One-Touch blood glucose meter and pathology of heart, kidney, and pancreas tissues were observed under a light microscope. The hyperinsulinaemic-euglycaemic clamp technique was applied to measure the increase of glucose infusion rate (GIR) of neoglitazone on the immune insulin-resistant rats induced by Bacillus Calmette-Guerin therapy decreased ( 14±s4)%, (55±24)%,and (28±7)% of blood glucose levels compared with CMC-Na+insulin group, respectively (P < 0.01) . In DB/DB mice, neoglitazone showed better reduction in blood glucose levels than those of model animals (P < 0.01) , and pathological studies indicated that neoglitazone attenuated the diabetic kidney and pancreas lesions. During a hyperinsulinaemic-euglycaemic clamp,neoglitaxone(10,30,and 100mg·kg-1·d-1,ig for 2 wk )-treated groups required significantly higher GIR to maintain basal glucose concentrations than model group (P < 0.01 ). CONCLUSION Neoglitazone could directly enhance insulin sensitivity and ameliorate insulin resistance in different diabetic animal models.