ABSTRACT
AIM: The aims of this study were to investigate the effects of calcium at the same concentration as that found in human milk on the viability, proliferation, and adhesion of MCF-7 human breast ductal carcinoma cells by exposing them to calcium at the same frequency as in breastfeeding. MATERIALS AND METHODS: High-concentration calcium was applied for 30 minutes every 4 hours for 24, 48, and 72 hours. Cell proliferation and viability were measured using a hemocytometer and the MTT cell viability assay. The effects of calcium treatment were evaluated by a comparison among a multiple-, single-dose calcium treatment, and a control group. RESULTS: We show that calcium at the same concentration as that in milk caused a decrease in the number of cells but did not affect cell viability. CONCLUSIONS: The results of this study suggest that calcium caused a lowering of the number of cells from the luminal surface of the breast by triggering proliferation under the condition of fluidity. Calcium and fluidity together serve to eliminate breast cancer stem cells during the lactation period. Effects of the other components of milk can be analyzed by the new method developed in this study.
Subject(s)
Breast Neoplasms/pathology , Breast/drug effects , Breast/pathology , Calcium/analysis , Calcium/pharmacology , Milk, Human/chemistry , Breast Feeding , Calcium/administration & dosage , Cell Adhesion/drug effects , Cell Proliferation/drug effects , Cell Survival/drug effects , Female , Humans , Lactation , MCF-7 Cells , PregnancyABSTRACT
BACKGROUND/AIM: There is no information on the dose-response relationship of curcumin on the hemodynamic variables of the heart at the organ level in isolated perfused rat hearts. We aimed to investigate the effects and mechanisms of curcumin on the hemodynamic variables of isolated perfused rat hearts. MATERIALS AND METHODS: Rats were randomly divided into 9 groups. The isolated rat heart was retrogradely perfused with modified Krebs-Henseleit solution. After the stabilization period, each group was administered one of the following treatments for 25 min: saline, dimethyl sulfoxide, and curcumin (0.2 µM, 1 µM, and 5 µM); atropine (1 µM); atropine (1 µM) + curcumin (1 µM); L-NAME (100 µM); or L-NAME (100 µM) + curcumin (1 µM). Hemodynamic variables of the heart were measured. RESULTS: Curcumin at dose of 1 µM decreased the heart rate (from 271 ± 11.1 to 200.4 ± 14.3 beats/min, P = 0.011) but increased end-diastolic pressure (from 7.0 ± 0.4 to 54.6 ± 7.9 mmHg, P = 0.0008). A dose of 5 µM curcumin caused a decrease in the developed pressure (from 87.58 ± 9.0 to 65.40 ± 7.0 mmHg, P = 0.047) but an increase in the end-diastolic pressure (from 6.8 ± 0.6 to 48.9 ± 7.7 mmHg, P = 0.005). Atropine (1 µM) reversed the effects of curcumin on the heart. CONCLUSION: Our results suggest that curcumin produces dose-dependent negative chronotropic and inotropic effects in isolated perfused rat hearts.
