Chunliang Liu1, Sheng Peng, Qingyang Li. 1. aDepartment of Anesthesiology, Seventh People's Hospital of Shanghai University of TCM bDepartment of Anesthesiology, Shanghai Songjiang District Central Hospital, Shanghai City, PR China.
Abstract
OBJECTIVE: Propofol is broadly utilized for maintaining anesthesia. Propofol affects neurodegeneration and neurogenesis by regulation of autophagy via effects on intracellular calcium homeostasis. The underlying molecular mechanism, however, is still unclear. METHODS: In the present research, we systematically analyzed the effect of propofol on mouse neuronal cells (cell line: HT-22). Cell Counting Kit-8 assays were utilized to examine cell proliferation. Flow cytometry was used to determine the levels of cell apoptosis. Quantitative real-time PCR and western blot were used to examine the relative mRNA and protein levels in mouse neuronal cells. RESULTS: Our results suggest that propofol inhibits proliferation and promotes apoptosis in neuronal cells. Moreover, overexpression of the transcriptional repressor RE-1 silencing transcription factor rescued the effect of propofol on neuronal cells. Additionally, the autophagy inhibitor 3-methyladenine also significantly reduced the effect of propofol on mouse neuronal cells. Finally, overexpression of RE-1 silencing transcription factor promoted the expression of brain-derived neurotrophic factor in mouse neuronal cells. CONCLUSION: Our research not only enhances our understanding of propofol on mouse neuronal cells but also uncovers a potential signaling pathway that may mediate the effects of propofol on neuronal cells.
OBJECTIVE:Propofol is broadly utilized for maintaining anesthesia. Propofol affects neurodegeneration and neurogenesis by regulation of autophagy via effects on intracellular calcium homeostasis. The underlying molecular mechanism, however, is still unclear. METHODS: In the present research, we systematically analyzed the effect of propofol on mouse neuronal cells (cell line: HT-22). Cell Counting Kit-8 assays were utilized to examine cell proliferation. Flow cytometry was used to determine the levels of cell apoptosis. Quantitative real-time PCR and western blot were used to examine the relative mRNA and protein levels in mouse neuronal cells. RESULTS: Our results suggest that propofol inhibits proliferation and promotes apoptosis in neuronal cells. Moreover, overexpression of the transcriptional repressor RE-1 silencing transcription factor rescued the effect of propofol on neuronal cells. Additionally, the autophagy inhibitor 3-methyladenine also significantly reduced the effect of propofol on mouse neuronal cells. Finally, overexpression of RE-1 silencing transcription factor promoted the expression of brain-derived neurotrophic factor in mouse neuronal cells. CONCLUSION: Our research not only enhances our understanding of propofol on mouse neuronal cells but also uncovers a potential signaling pathway that may mediate the effects of propofol on neuronal cells.