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Effects of propofol on human brain organoids at different maturational stages

ABSTRACT: Human brain organoids were derived from the H1 human embryonic stem cell line and exposed at different developmental stages to propofol (50 µM) for 3 days in vitro (div). Human brain organoids were investigated in four experimental groups at two developmental stages, 60 div and 90 div, including mock-treated groups as control and propofol-treated groups (from 47-50 div or 77-80 div, n=5 each). Our results suggest that propofol affects synapse-associated gene expression and neuronal activity differently at specific developmental stages.

ORGANISM(S): Homo sapiens

PROVIDER: GSE294524 | GEO | 2026/02/18

REPOSITORIES: GEO

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Propofol Differentially Modulates Neurodevelopmental Processes in Region-Specific Human Brain Organoids

Project description:Background: Propofol, a commonly used anesthetic, has controversial effects on fetal neurodevelopment. This study explores the hypothesis that propofol exerts region- and time-specific effects on distinct brain regions, with implications for clinical safety during pregnancy. Methods: Human dorsal forebrain (hCS) and ventral forebrain (hSS) organoids were exposed to 20 μM propofol for 6 hours on day 11 (D11). Morphological changes, including diameter and surface area, were analyzed at D11, D18, and D25. Immunofluorescence and PCR analyses were conducted at early (D18/25), middle (D40), and late stages (D80) post-intervention. Electrophysiological analyses were performed from D40 to D70, and bulk RNA-seq analyses were conducted on organoids at D18 to assess transcriptional changes. Results: Propofol exhibited region-specific effects on hCS and hSS organoids. In hCS organoids, excitatory neuron markers were consistently reduced at all stages, while in hSS organoids, inhibitory neuron markers were transiently affected at early stages but recovered over time. Electrophysiological analysis revealed increased action potential incidence in hCS organoids, indicating enhanced neuronal excitability despite decreased excitatory neuron markers. Transcriptomic analysis demonstrated metabolic reprogramming, including improved oxygen supply and a shift toward efficient aerobic pathways, alongside modulation of developmental signaling pathways. Conclusions: Propofol exerts region- and time-specific effects on neural development, involving both neuronal maturation and metabolic adaptation. These findings emphasize the need for careful evaluation of anesthetic safety in pregnant women and its potential long-term neurodevelopmental consequences.

2026-01-16 | GSE287509 | GEO

human iPSC derived cerebral organoids: Propofol treated vs. DMSO control

Project description:LncRNA and mRNA profiling of human iPSC derived cerebral organoids (Propofol treated vs. DMSO control) were determined. LncRNA and mRNA profiling of human iPSC derived cerebral organoids (Propofol treated vs. DMSO control) were determined.

2025-12-30 | GSE271591 | GEO

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.

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

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human iPSC derived cerebral organoids: Propofol treated vs. DMSO control

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Suppressive effect of the anesthetic Propofol on the T cell function and T cell-dependent immune responses

Project description:General anesthesia is thought to suppress the immune system and negatively affect postoperative infection and the long-term prognosis of cancer. However, the mechanism underlying immunosuppression induced by general anesthetics remains unclear. In this study, we focused on propofol, which is widely used for sedation under general anesthesia and intensive care and examined its effects on the T cell function and T cell-dependent immune responses. We found that propofol suppressed T cell glycolytic metabolism, differentiation into effector T cells, and cytokine production by effector T cells. CD8 + T cells activated and differentiated into effector cells in the presence of propofol in vitro showed reduced antitumor activity. Furthermore, propofol treatment suppressed the increase in the number of antigen-specific CD8 + T cells during Listeria infection. In contrast, the administration of propofol improved inflammatory conditions in mouse models of inflammatory diseases, such as OVA-induced allergic airway inflammation, hapten-induced contact dermatitis, and experimental allergic encephalomyelitis. These results suggest that propofol may reduce tumor and infectious immunity by suppressing the T cell function and T cell-dependent immune responses while improving the pathogenesis and prognosis of chronic inflammatory diseases by suppressing inflammation.

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