Cytisine induces apoptosis of HepG2 cells
Autor: | Dong‑Yu Shang, Lian‑Fang Zhang, Zhi‑Feng Chen, Jing‑Hui Yang, Yu‑Bin Ji, Xin Wang, Bo Jiang, Lei Yu, Yong‑Xue Sun |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Cancer Research Cell Survival Apoptosis Biology Biochemistry Flow cytometry 03 medical and health sciences Cytisine chemistry.chemical_compound Alkaloids 0302 clinical medicine Downregulation and upregulation Genetics medicine Humans Rhodamine 123 MTT assay Cytotoxicity Cell Shape Molecular Biology Membrane Potential Mitochondrial medicine.diagnostic_test Caspase 3 Cytochrome c Cytochromes c Hep G2 Cells Flow Cytometry Azocines Cell biology 030104 developmental biology Oncology chemistry 030220 oncology & carcinogenesis Cancer cell biology.protein Molecular Medicine Quinolizines |
Zdroj: | Molecular Medicine Reports. 16:3363-3370 |
ISSN: | 1791-3004 1791-2997 |
Popis: | Cytisine is a quinolizidine alkaloid, which has been reported to be among the major bioactive components of Sophora alopecuraides L. Quinolizidine alkaloids have previously been demonstrated to inhibit the proliferation of several types of tumor cells. However, few studies have investigated the effects of cytisine on cancer cells. The present study was performed to further investigate the molecular mechanisms underlying cytisine‑induced apoptosis of HepG2 human hepatocellular carcinoma cells. The results of an MTT assay demonstrated that cytisine inhibited the growth of HepG2 cells in a dose‑dependent manner. In addition, the induction of apoptosis was detected, as determined by morphological observation and flow cytometry. As determined by fluorescence microscopy, apoptotic morphological alterations were detected following cytisine administration. Flow cytometric analyses demonstrated that cytisine induced cytotoxicity through apoptosis‑like mechanisms in HepG2 cells. Furthermore, western blot analysis was performed to investigate the release of cytochrome c (Cyt‑c) and activation of the caspase cascade, and the results indicated that treatment of HepG2 cells with cytisine induced caspase‑dependent apoptosis via the release of Cyt‑c from the mitochondria, upregulation of caspase‑3 and downregulation of pro‑caspase‑3. These results indicated that cytisine may induce apoptosis of HepG2 cells through the mitochondrial pathway. |
Databáze: | OpenAIRE |
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