Objective： To observe the effect of Shugan Liangxue Decoction（舒肝凉血方, SGLXD） on estrogen receptor α（ERα） in human breast cancer cells. Methods： The effect of SGLXD（0.85–5.10 mg/m L） on the proliferation...Objective： To observe the effect of Shugan Liangxue Decoction（舒肝凉血方, SGLXD） on estrogen receptor α（ERα） in human breast cancer cells. Methods： The effect of SGLXD（0.85–5.10 mg/m L） on the proliferation of breast cancer cells were evaluated by 3-（4,5-dimethyl-2-thiazolyl）-2,5-diphenyl-2-H-tetrazolium bromide（MTT） assay. The nuclear ERα protein levels in MCF-7, T47 D and ZR-75-1 cells which treated by SGLXD for 24 h were examined by western blot and immunofluorescence assay. MCF-7 and MDA-MB-231 cells were treated by 17β-estradiol（E2） with or without SGLXD, for 24 h, and the E2 targeted genes c-myc and bcl-2 protein product was evaluated by western blot. Results： SGLXD showed dose-dependent inhibition on the proliferation of MCF-7, T47 D and ZR-75-1 cells, but did not inhibit the proliferation of MDA-MB-231 cells. Furthermore, the promotive effect on cell growth induced by E2 was also significantly inhibited by SGLXD treatment. With the treatment of 1.70, 3.40, 5.10 mg/m L SGLXD, the nuclear ERα protein level was reduced to 88.1%, 70.4% and 60.9% in MCF-7 cells, and was decreased to 43.0%, 38.4% and 5.9% in ZR-75-1 cells as compared with the control group. In T47 D cells, the nuclear ERα protein was down-regulated to 51.3% and 4.3% by 3.40 and 5.10 mg/m L SGLXD treatment. The down-regulative effect of SGLXD on nuclear ERα was confirmed by immunofluorescence assay. SGLXD decreased the protein product of c-myc and bcl-2. Conclusions： SGLXD may exhibit selective inhibition effect on the proliferation of ER positive breast cancer cells. SGLXD reduced the nuclear ERα expression and the protein product of E2 target gene c-myc and bcl-2.展开更多
基金Supported by the National Natural Science Foundation of China(No.30973906)
文摘Objective： To observe the effect of Shugan Liangxue Decoction（舒肝凉血方, SGLXD） on estrogen receptor α（ERα） in human breast cancer cells. Methods： The effect of SGLXD（0.85–5.10 mg/m L） on the proliferation of breast cancer cells were evaluated by 3-（4,5-dimethyl-2-thiazolyl）-2,5-diphenyl-2-H-tetrazolium bromide（MTT） assay. The nuclear ERα protein levels in MCF-7, T47 D and ZR-75-1 cells which treated by SGLXD for 24 h were examined by western blot and immunofluorescence assay. MCF-7 and MDA-MB-231 cells were treated by 17β-estradiol（E2） with or without SGLXD, for 24 h, and the E2 targeted genes c-myc and bcl-2 protein product was evaluated by western blot. Results： SGLXD showed dose-dependent inhibition on the proliferation of MCF-7, T47 D and ZR-75-1 cells, but did not inhibit the proliferation of MDA-MB-231 cells. Furthermore, the promotive effect on cell growth induced by E2 was also significantly inhibited by SGLXD treatment. With the treatment of 1.70, 3.40, 5.10 mg/m L SGLXD, the nuclear ERα protein level was reduced to 88.1%, 70.4% and 60.9% in MCF-7 cells, and was decreased to 43.0%, 38.4% and 5.9% in ZR-75-1 cells as compared with the control group. In T47 D cells, the nuclear ERα protein was down-regulated to 51.3% and 4.3% by 3.40 and 5.10 mg/m L SGLXD treatment. The down-regulative effect of SGLXD on nuclear ERα was confirmed by immunofluorescence assay. SGLXD decreased the protein product of c-myc and bcl-2. Conclusions： SGLXD may exhibit selective inhibition effect on the proliferation of ER positive breast cancer cells. SGLXD reduced the nuclear ERα expression and the protein product of E2 target gene c-myc and bcl-2.
