Effects of lutein on viability of breast cancer cells
10.3969/j.issn.1000-4718.2018.05.025
- VernacularTitle:叶黄素对乳腺癌细胞活力的影响
- Author:
Jing-Zhi CHANG
1
;
Chen WANG
;
Yi-Chuan LI
;
Qing LIU
;
Yong-Jie SHEN
;
Kun LU
;
Ya-Li GUO
;
Shan-Feng ZHANG
;
Ming-Chen WANG
Author Information
1. 商丘医学高等专科学校生物化学与分子生物学教研室
- Keywords:
Lutein;
Breast cancer;
Cell viability;
NF-κB signaling pathway
- From:
Chinese Journal of Pathophysiology
2018;34(5):930-933
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the effect of lutein on the viability of breast cancer cells and its possible mech -anism.METHODS:The human breast cancer T47D cells were divided into control group and lutein(6.25,12.5,25,50 mg/L)treatment groups.The effect of lutein on the viability of T47D cells was measured by MTT assay.The mRNA ex-pression of nuclear factor erythroid 2-related factor 2(Nrf2),glutathione peroxidase 1(GPx1)and superoxide dismutase 2 (SOD2)was detected by RT-qPCR.Fluorescent probes DCFH-DA was used to determine the production of reactive oxygen species(ROS).The protein expression of Nrf2 and p65 was determined by Western blot.RESULTS: The MTT results showed that lutein inhibited T47D breast cancer cell viability in a dose-and time-dependent manner.The RT-qPCR results showed that the mRNA levels of Nrf2, GPx1 and SOD2 were higher in lutein treatment groups than those in the control group(P<0.05),and with the increased concentrations and extension of intervention time of lutein, the relative mRNA levels were all increased.The ROS levels were significantly decreased in the lutein-treated groups(P<0.05).The results of Western blot demonstrated that the protein expression of Nrf 2 was significantly increased(P<0.05), and p65 protein was decreased(P<0.05)in a dose-dependent manner with lutein treatment for 48 h.CONCLUSION: Lutein signifi-cantly inhibits the viability of breast cancer cells,and the inhibition roles may be related to up-regulation of the expression of Nrf2,antioxidant enzymes GPx1 and SOD2 mRNA expression and down-regulation of oxidative stress,thus blocking the NF-κB signaling pathway.
