Effect of rosmarinic acid from Sarcandra glabra in inhibiting proliferation and migration and inducing apoptosis of MDA-MB-231 cells via regulation of expressions of Bcl-2 and Bax.
10.19540/j.cnki.cjcmm.20180508.001
- Author:
Hong LI
1
;
Hai-Lin ZHUANG
1
;
Jun-Jin LIN
2
;
Yue-Fen ZHANG
3
;
Hui HUANG
3
;
Ting LUO
3
;
Wen-Tao YU
3
;
Feng NI
3
Author Information
1. Department of Health Management, Fujian Health College, Fuzhou 350101, China.
2. Sharing Technology Center, Fujian Medical University, Fuzhou 350122, China.
3. Biomedical Engineering Technology Center, Fujian Health College, Fuzhou 350101, China.
- Publication Type:Journal Article
- Keywords:
Bax;
Bcl-2;
MCF-7;
MDA-MB-231;
Sarcandra glabra;
apoptosis;
rosmarinic acid
- From:
China Journal of Chinese Materia Medica
2018;43(16):3335-3340
- CountryChina
- Language:Chinese
-
Abstract:
Rosmarinic acid is one of anti-tumor ingredients in the Sarcandra glabra. After treatment with 0, 10, 30, 90, 270 and 810 μmol·L⁻¹ rosmarinic acid for 24, 48, 72 hours respectively, the inhibitory effects on MCF-7 and MDA-MB-231 cells were observed by CCK-8 and cell wound healing test. No significant inhibition effecton proliferation and migration was observed in MCF-7 cell. However, 90, 270 and 810 μmol·L⁻¹ rosmarinic acid could inhibit the proliferation and migration of MDA-MB-231 cells in a dose-dependent and time-dependent manner. Flow cytometry was further used to detect apoptosis ratios of MDA-MB-231 cells after Annexin V-FITC/PI staining, and significant apoptosis was observed after rosmarinic acid treatment. Real-time PCR and Western blot tests were carried out to detect the expressions of apoptosis-related genes. The down-regulation of the Bcl-2 expression and the up-regulation of the Bax expression were observed in MDA-MB-231 cells after rosmarinic acid treatment. The results suggested that rosmarinicacid can inhibit the proliferation and migration, and induce the apoptosis of MDA-MB-231 cells, which may be correlated with the down-regulation of Bcl-2 gene and the up-regulation of Bax gene.
