期刊
DRUG DESIGN DEVELOPMENT AND THERAPY
卷 14, 期 -, 页码 1561-1569出版社
DOVE MEDICAL PRESS LTD
DOI: 10.2147/DDDT.S229520
关键词
metformin; propofol; Cav-1; apoptosis
资金
- Nantong Health and Family Planning Commission [MA2019004]
- Top Six Types of Talents' Financial Assistance of Jiangsu Province [2019-WSW-199]
- Nantong Science and Technology Project [JCZ18004]
Objective: To elucidate the neuroprotective function of metformin in suppressing propofol-induced apoptosis of HT-22 cells. Methods: HT-22 cells were treated with 0, 10 or 100 mu mol/L propofol, followed by determination of their proliferative ability. Subsequently, changes in proliferation and apoptosis of propofol-treated HT-22 cells induced with metformin were assessed. Apoptosis-associated genes in HT-22 cells were detected by Western blot. At last, regulatory effects of Cav-1 on propofol and metformin-treated HT-22 cells were examined. Results: Propofol treatment dose-dependently decreased proliferative ability and increased apoptosis ability in HT-22 cells, which were partially blocked by metformin administration. Upregulated Bcl-2 and downregulated Bax were observed in propofol-treated HT-22 cells following metformin administration. In addition, Cav-1 level in HT-22 cells was regulated by metformin treatment. Notably, metformin reversed propofol-induced apoptosis stimulation and proliferation decline in HT-22 cells via downregulating Cav-1. Conclusion: In our study, we found that propofol could induce apoptosis of HT-22 cells and metformin could rescue the apoptosis effect regulated by propofol. Then, we found that metformin protects propofol-induced neuronal apoptosis via downregulating Cav-1.
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