Retracted: Propofol exerts neuroprotective functions by down‐regulating microRNA‐19a in glutamic acid‐induced PC12 cells
| Autor: | Wenqi Xin, Shashuang Yu, Qiliang Jiang, Aixiang Li |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
medicine.diagnostic_test Chemistry Clinical Biochemistry Autophagy AMPK General Medicine Transfection Pharmacology Biochemistry Flow cytometry 03 medical and health sciences 030104 developmental biology 0302 clinical medicine Western blot Apoptosis 030220 oncology & carcinogenesis medicine Molecular Medicine Viability assay PI3K/AKT/mTOR pathway |
| Zdroj: | BioFactors. 46:934-942 |
| ISSN: | 1872-8081 0951-6433 |
| DOI: | 10.1002/biof.1607 |
| Popis: | Background Propofol, a kind of intravenous sedative drug, is certified that exerts anti-inflammation and antitumor functions. However, the influence of propofol in cerebral injury and the corresponding mechanism remains unexplained, that our article focuses on. Methods PC12 cells were treated with propofol and exposed in glutamic acid (Glu) solutions. Cell viability, apoptotic potential, apoptosis-related and autophagy-linked proteins were tested via CCK-8, flow cytometry, and western blot assays. Reverse transcription-quantitative real-time PCR was utilized to test miR-19a expression in Glu-stimulated cells. Next, miR-19a mimic transfection was used to assess the effects of miR-19a on cell apoptosis and autophagy in Glu or propofol treated cells. Finally, western blot was performed to test AMPK and mTOR pathways. Results Glu exposure promoted cell apoptosis and autophagy of PC12 cells, while propofol attenuated cell apoptosis and autophagy triggered by Glu. Additionally, propofol decreased the miR-19a expression in Glu-stimulated PC12 cells. Meanwhile, over-expression of miR-19a reversed the effects of propofol on Glu-induced cell apoptosis and autophagy. Moreover, propofol potentiated AMPK and mTOR pathways in Glu-stimulated PC12 cells via impeding miR-19a expression. Conclusions These finding revealed that propofol relieved Glu-triggered apoptosis and autophagy of PC12, and activated AMPK and mTOR pathways by suppressing miR-19a expression. |
| Databáze: | OpenAIRE |
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