Role of mitochondria damage in quercetin induced MCF-7 cell apoptosis / 中国药学杂志
Chinese Pharmaceutical Journal
;
(24): 1765-1770, 2016.
Article
in Chinese
| WPRIM
| ID: wpr-858938
ABSTRACT
OBJECTIVE:
To investigate the mitochondrial damage and the possible mechanism in the process of MCF-7 cell apoptosis which induced by quercetin.METHODS:
The cell apoptosis model was established with MCF-7 cells induced by quercetin. The morphological characteristics of apoptotic MCF-7 cells were observed by transmission electron microscope. Fluorescent probes DCFH-DA and Fluo-8-AM were used to detect the invaded cells' reactive oxygen species (ROS) and intracellular Ca2+concentration, respectively. The calcium channel blockers of extracellular and intracellular were used to inhibit apoptosis induced by quercetin in MCF-7 cells, the cellular apoptosis rates of which were measured by flow cytometry. Western blot assay was used to detect the expressions of Cyt C.RESULTS:
Quercetin can induce MCF-7 cell mitochondria apoptosis. The spherical swelling, mitochondrial crest disappear and the formation of cavity were happened to those cells. Intracellular ROS and Ca2+ increased. The apoptosis induced by quercetin can be inhibit by intracellular calcium blockers ryanodine. After incubation with ryanodine, apoptosis rates fell by 55.4% at 24 h, 55.4% at 48 h and 39.9% at 72 h, respectively. The cell apoptosis induced by quercetin was not inhibited by EDTA. The expression of Cyt C was increased in the cytoplasm but not mitochondria after cultured the MCF-7 cell with EDTA.CONCLUSION:
The mitochondrial damage plays an important role in the MCF-7 apoptosis which induced by quercetin, and its possible mechanism may related to the elevated levels of ROS and the release of Ca2+ and Cyt C in the cytoplasm. Meanwhile, Cyt C in the cytosol is potential critical signaling molecular in the process of apoptosis.
Full text:
Available
Index:
WPRIM (Western Pacific)
Type of study:
Prognostic study
Language:
Chinese
Journal:
Chinese Pharmaceutical Journal
Year:
2016
Type:
Article
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