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Pharmacodynamics of propofol in painless enteroscopy in different ages people

ABSTRACT: Interventions: super elderly patient group:Patient aged from 76 to 89 receive propofol TCI;elderly patient group:Patient aged from 65 to 75 receive propofol TCI ;young patient group:Patient aged from 30 to 64 receive propofol TCI Primary outcome(s): Body movement Study Design: Cohort study

DISEASE(S): Enteritis, Intestinal Tumor

PROVIDER: 2678135 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Effects of Propofol Treatment in Neural Progenitors Derived from Human Induced Pluripotent Stem Cells

Project description:Propofol is an intravenous anesthetic that has been widely used in the clinical setting. Besides its anesthetic effects, propofol has been reported to influence the regulation of autonomic system. Controversies exist with regards to whether propofol exposure is safe for pregnant women and young children. The recent emergence of human induced pluripotent stem cells (hiPSCs) has provided a promising and theoretically inexhaustible source of neural progenitor cells (NPCs) for drug testing, which could be extended to in vitro experiments for anesthetics such as propofol. NPCs derived from three hiPSC lines, NES-GFP (a NESTIN-GFP reporter), USCK7 (iPSCs derived from urine derived cells), and ND2-0 (NIH), were treated with propofol at different concentrations (20, 50, 100 and 300 µM) for 6 h or 24 h. Early and late cell injury, cell proliferation and apoptosis were evaluated. Comparison of genome-wide gene expression profiles was performed for propofol-treated and untreated control iPSC-NPCs. Propofol treatment of NPCs for 6 h at the clinically relevant concentration (20 or 50 µM) did not affect cell viability, apoptosis, or proliferation, while propofol at higher concentration (100 or 300 µM) decreased NPC viability and induced apoptosis. Prolonged treatment of propofol for 24 h significantly decreased cell viability. In addition, 20 µM propofol treatment for 6 h did not alter global gene expression. Higher concentration of propofol exerted potential cytotoxicity via multiple cellular mechanisms. In summary, propofol treatment at commonly practiced clinical doses for 6 h did not have adverse effects on hiPSC-derived NPCs. In contrast, longer exposure and/or higher concentration of propofol treatment could decrease NPC viability and induce apoptosis.

2017-07-21 | GSE101724 | GEO

Disturbance of key cellular subproteomes upon propofol treatment is associated with increased permeability of the blood-brain barrier

Project description:Background: Propofol is a short-acting anesthetic, which is often used for induction and maintenance of general anesthesia, sedation for mechanically ventilated adults and procedural sedation. Several side effects of propofol are known and a substantial number of patients suffer from post-operative delirium after propofol application. In this study, we analyzed the effect of propofol on the function and protein expression profile on a proteome-wide scale. Methods: We cultured human brain microvascular endothelial cells in the absence and presence of propofol and analyzed the permeability of the blood-brain barrier (BBB) by fluorescein passage and protein expression on a proteome-wide scale by mass spectrometry. Results: Propofol interfered with the function of the blood-brain barrier. This was not due to de-creased adhesion of propofol-treated human brain microvascular endothelial cells. The proteomic analysis revealed that some key pathways in these cells were disturbed, such as oxygen metabolism, DNA damage recognition and response to stress. Conclusions: Propofol has strong effects on protein expression which could explain several side effects of propofol.

2022-10-13 | PXD033856 | Pride

Propofol alters the mRNA profile in the developing mouse hippocampus

Project description:Propofol has been found to be toxic to developing neurons. The goal of the current study was to nominate novel genes predicted to underly the neurotoxicity, and use these candidates for future functional pathway assessment

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Enhanced hippocampal neurogenesis mediated by PGC-1α-activated OXPHOS after neonatal low-dose Propofol exposure

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Enhanced hippocampal neurogenesis mediated by PGC-1α-activated OXPHOS after neonatal subclinical dose of Propofol exposure revealed by single-nuclei transcriptomic profiling

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Gene expression of brain regions activated by sevoflurane and propofol

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2021-12-22 | GSE192399 | GEO

Gene expression of brain regions activated by sevoflurane and propofol

Project description:Gene expression of brain regions activated by sevoflurane and propofol

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Propofol alters the mRNA profile in the developing mouse hippocampus

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UPLC-MS-Based Serum Metabolic Profiling Reveals Potential Biomarkers for Predicting Propofol Responsiveness in Females

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2021-09-29 | MTBLS2311 | MetaboLights

Exploring the Biological Mechanisms of Severe COVID-19 in the Elderly: Insights from an Aged Mouse

Project description:Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in a global health crisis, particularly affecting the elderly, who are more susceptible to severe outcomes. However, definitive parameters or mechanisms underlying the severity of COVID-19 in elderly people remain confused. Thus, this study seeks to elucidate the mechanism behind the increased vulnerability of elderly individuals to severe COVID-19. We employed an aged mouse model with a mouse-adapted SARS-CoV-2 strain to mimic the severe symptoms observed in elderly patients with COVID-19. Comprehensive analyses of the whole lung were performed using transcriptome and proteome sequencing, comparing data from aged and young mice. For transcriptome analysis, bulk RNA sequencing was conducted using an Illumina sequencing platform. Proteomic analysis was performed using mass spectrometry following protein extraction, digestion, and peptide labeling. We analyzed the transcriptome and proteome profiles of young and aged mice and discovered that aged mice exhibited elevated baseline levels of inflammation and tissue damage repair. After SARS-CoV-2 infection, aged mice showed increased antiviral and inflammatory responses; however, these responses were weaker than those in young mice, with significant complement and coagulation cascade responses. In summary, our study demonstrates that the increased vulnerability of the elderly to severe COVID-19 can be attributed to an attenuated antiviral response and the overactivation of complement and coagulation cascades.

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