RETRACTED: Ginkgolides B alleviates hypoxia-induced PC-12 cell injury by up-regulation of PLK1
| Autor: | Jian Gao, Tuo Zhang, Yingying Han, Chunyang Kang, Mingyang Kang, Hui Jin |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
MAPK/ERK pathway Cell cycle checkpoint Apoptosis Cell Cycle Proteins Protein Serine-Threonine Kinases PC12 Cells 03 medical and health sciences Lactones Phosphatidylinositol 3-Kinases 0302 clinical medicine Proto-Oncogene Proteins Animals MTT assay Viability assay Extracellular Signal-Regulated MAP Kinases Protein kinase B PI3K/AKT/mTOR pathway Pharmacology Molecular Structure Chemistry Cell Cycle General Medicine Cell cycle MAP Kinase Kinase Kinases Cell biology Rats Up-Regulation Oxygen 030104 developmental biology Ginkgolides Gene Expression Regulation 030220 oncology & carcinogenesis Reactive Oxygen Species Proto-Oncogene Proteins c-akt |
| Zdroj: | Biomedicinepharmacotherapy = Biomedecinepharmacotherapie. 115 |
| ISSN: | 1950-6007 |
| Popis: | Background Finding novel agent for cerebral ischemia therapy is urgently required. In our present study, we aimed to investigate the regulatory mechanism of Ginkgolides B (GB) in hypoxia-injured PC-12 cells. Methods PC-12 cells were exposed to hypoxia and administrated with GB. Cell viability was detected by MTT assay. Flow cytometry assay was conducted for the detection of cell apoptosis, ROS generation and cell cycle assay. The changes of protein levels of Bax, Pro/Cleaved-Caspase-3, CyclinD1, CDK4, CDK6, PI3K/AKT and MEK/ERK pathways were detected by Western blot. Transfection was conducted for Polo-like kinase 1 (PLK1) knockdown. Results Hypoxia-induced decrease of cell viability and increase of ROS generation, apoptosis and cell cycle arrest were ameliorated by GB. Hypoxia disposition hindered PI3 K/AKT and MEK/ERK signaling pathways while GB had the opposite effects. Then we observed that hypoxia exposure suppressed PLK1 expression while GB increased PLK1 expression dose-dependently. Knockdown of PLK1 attenuated the neuroprotective effects of GB on hypoxia-injured PC-12 cells and also inhibited PI3 K/AKT and MEK/ERK pathways. Conclusion The above observations corroborated that GB alleviated hypoxia-induced PC-12 cell injury by up-regulation of PLK1 via activating PI3K/AKT and MEK/ERK pathways. These findings implied the neuro-protective impacts in hypoxia-injured PC-12 cells. |
| Databáze: | OpenAIRE |
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