Mechanism of gastric carcinoma cell apoptosis induced by chlorogenic acid-like compounds extracted from Broussonetia papyrifera
10.7501/j.issn.0253-2670.2018.22.019
- Author:
Ze-Xin ZHU
1
Author Information
1. College of Agricultural, Guangdong Ocean University
- Publication Type:Journal Article
- Keywords:
Broussonetia papyrifera (Linn.) L'Hér. ex Vent.;
Cell apoptosis;
Chlorogenic acid-like compounds;
MAPK signal pathway;
Oxidative stress
- From:
Chinese Traditional and Herbal Drugs
2018;49(22):5345-5351
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the mechanism of gastric carcinoma cell SGC-7901 apoptosis induced by chlorogenic acid-like compounds extracted from Broussonetia papyrifera (CALCBP) bark. Methods The SGC-7901 cells were used to evaluate the anti-tumour activity of the extract in vivo, and the proliferation of cells was examined by MTT assay. The cell morphological changes of cells were observed by DAPI staining; The cell apoptosis and the cell cycle were detected respectively by flow cytometry after PI and Annexin V/PI staining; The intracellular ROS were determined under the fluorescence microscope using DCHF-DA probe, the changes of mitochondrial membrane potential were observed by JC-1 staining. The protein expression of p53, Bcl-2, Bax, and Cytochrome C, p-p38, p-JNK, JNK, p-ERK, ERK were analyzed by Western blotting. Results The proliferation of SGC-7901 cells was inhibited significantly by CALCBP in dose-dependent and time-dependent manner, the condensed chromosome and apoptotic body can be observed in the treated cells and the cell cycle was arrested in G2/M phase, the mitochondrial membrane potential was significantly decreased, whereas the cellular ROS levels of the treated cells were significantly increased. Moreover, the protein expression of p53, Bax, Cytochrome C, and p-p38 were significantly up-regulated and p-ERK and Bcl-2 expression were significantly down-regulated. Conclusion The apoptosis of gastric cancer cell SGC-7901 induced by CALCBP was probably related to oxidative stress of the cell mitochondrial via p38-MAPK and ERK-MAPK signal pathways.
