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Propofol

Manufactured by Merck Group
Sourced in United States, Germany, United Kingdom, China, Sao Tome and Principe

Propofol is a sterile, injectable emulsion used as a general anesthetic and sedative agent. It is a colorless to slightly yellow oil-in-water emulsion. Propofol is intended for intravenous administration.

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155 protocols using propofol

1

Oxytocin and Anesthetic Effects on Tissue

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All drugs and solutions were prepared immediately before each experiment was performed. Oxytocin (Sigma-Aldrich, St. Louis, MO, USA) was added directly to the organ baths to a final concentration of 20 nM, with reference to a previous study [13 (link)]. The effects of propofol (Sigma-Aldrich) were evaluated at cumulative concentrations of 10−7 M, 10−6 M, and 10−5 M. Given that more than 95% of propofol (2–5 × 10−5 M) in the blood is bound to plasma protein [28 (link)], a free propofol concentration of 4–10 × 10−7 M in vitro would be comparable to 9–10 µg/ml of propofol in vivo [29 (link)]. Because the therapeutic range of plasma propofol is 2–9 µg/ml, the effective propofol concentrations tested in this study were considered close to the free concentrations clinically observed in serum. The effects of dexmedetomidine (Maruishi, Osaka, Japan) were evaluated at cumulative concentrations of 10−9 M, 10−8 M, and 10−7 M. Ebert et al. reported that the therapeutic plasma concentration of dexmedetomidine for sedation ranges from 0.7 to 1.2 ng/ml [30 (link)]. Based on previous studies, we selected dexmedetomidine concentrations that would reach therapeutic plasma concentrations. Sevoflurane (Maruishi) was introduced into the gas mixture using agent-specific vaporizers (Vapor 19.3, Dragerwerk, Lubeck, Germany). All other reagents used in the experiments were of analytical grade.
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2

PC-12 Cell Culture under Normoxia and Hypoxia

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The PC-12 cells (ATCC® CRL-1721™) were obtained from American Type Culture Collection (ATCC; Manassas, VA, USA). Cells were maintained in RPMI 1640 medium (Hyclone, Logan, UT, USA) containing 10% heat-inactivated horse serum (Hyclone) and 5% fetal bovine serum (Hyclone). For incubation under normoxia, cells were grown in a humidified incubator at 37 °C with 5% CO2 and 95% air. For incubation under hypoxia, cells were subjected into a humidified anaerobic chamber containing 94% N2, 5% CO2, and 1% O2 for 48 h. Propofol (Sigma-Aldrich, St. Louis, MO, USA) was primarily dissolved in dimethyl sulfoxide (DMSO) shortly before use, and it was diluted into RPMI 1640 medium to yield a final Propofol concentration of 10 μg/mL. Propofol (10 μg/mL) was applied to stimulate PC-12 cells for 48 h. The final concentration of DMSO in the control group and Propofol group was 0.1%. The culture medium was refreshed every other day.
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3

Propofol Modulates Cardiomyocyte Response to LPS

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Cardiomyocytes were divided into the following groups: i) Control, cardiomyocytes cultured in serum-free maintenance medium; ii) propofol, cardiomyocytes treated with propofol (Sigma-Aldrich; Merck KGaA; 12.5, 25, 50 or 100 µM) for 6, 12, 24 or 48 h; iii) LPS, cardiomyocytes stimulated with 1 µg/ml LPS (Escherichia coli 055:B5; Sigma-Aldrich; Merck KGaA) for 4 h; iv) propofol + LPS, cardiomyocytes treated with propofol (12.5, 25, 50 or 100 µM) for 6, 12, 24 or 48 h then stimulated with 1 µg/ml LPS for 4 h; v) propofol + LPS + siRNA, cardiomyocytes transfected with 100 nM siNC, siHBGB1 or siPPARγ for 24 h, treated with propofol (50 µM) for 24 h and then stimulated with 1 µg/ml LPS for 4 h; vi) propofol + LPS + inhibitor, cardiomyocytes pretreated with recombinant rat HMGB1 (rHMGB1; Chimerigen Laboratories; 100 ng/ml) or GW9662 (a PPARγ activation inhibitor; MedChemExpress; 10 µM) for 30 min followed by treatment with propofol (50 µM) for 24 h and then stimulation with 1 µg/ml LPS for 4 h. All the treatments were incubated at 37°C in a humidified atmosphere containing 5% CO2.
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4

Rat Model of Propofol and Esketamine

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Forty-eight Sprague Dawley rats (male, 6–8 weeks, 240–280 g) were purchased from Vital River (Beijing, China).
The rats were randomly divided into six groups: control, control + esketamine, propofol, propofol + esketamine, propofol + esketamine + IgG and propofol + esketamine + anti-BDNF (n = 8/group). Rats in the propofol-treated groups were intraperitoneally injected with 50 mg/kg propofol (Sigma–Aldrich, Louis, MO, USA), followed by an injection of 50 mg/kg propofol again after 1 h when the rat righting reflex recovered [19 (link)]. Rats in the control group were administrated with 100 mg/kg intralipid [19 (link)]. Thirty minutes after propofol injection, rats in the esketamine-treated groups were intraperitoneally injected with 15 mg/kg esketamine (Cristalia, Brazil) [20 ]. Normal saline (NS) was used as a control for esketamine.
In some experiments, to examine the role of the BDNF/TrkB/PI3K signaling pathway, anti-BDNF was used for BDNF knockdown assays. Rats were intranasally administrated with anti-BDNF or control IgG (100 μg/kg) [21 (link)] using a sterile 26-G Hamilton microsyringe (Hamilton Company, Reno, NV, USA) 30 min before propofol treatment.
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5

Modulation of Tau Phosphorylation by TNF-α and Propofol

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Recombinant mouse TNF-α was obtained from Sigma-Aldrich (St. Louis, MO, USA) and was reconstituted with sterile water to a stock concentration of 0.1 mg/mL. To investigate the effect of TNF-α on p-Tau accumulation, neurons were exposed to different concentrations of TNF-α (10, 20, 40, 80, and 160 ng/mL) for different durations (1, 2, 4, and 8 h). By measuring the expression and phosphorylation of Tau protein, we aimed to determine the optimal condition, under which TNF-α exerted significant effect on the accumulation of p-Tau.
To investigate the protective effects of propofol against TNF-α in hippocampal neurons, we incubated neurons with different concentrations (1, 5, 10, 25, 50, and 100 μM) of propofol (Sigma-Aldrich, St Louis, MO, USA) or its solvent 0.1% dimethyl sulfoxide (DMSO, Sigma-Aldrich, St Louis, MO, USA) for 1 h followed by TNF-α treatment (with the presence of propofol or DMSO). By observing the expression and phosphorylation of Tau protein, we intended to identify the optimal concentration, at which propofol exerted protective effects against p-Tau accumulation.
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6

Investigating Propofol's Effects on Cervical Cancer Cells

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Propofol (Sigma-Aldrich, St. Louis, MO, USA) was dissolved in DMSO (Sigma-Aldrich) and made up with the culture medium until the final dose of Dimethyl sulfoxide (DMSO; Sigma-Aldrich) <0.1%. Then, HeLa and SiHa cells were treated with 1 µg/mL, 5µg/mL, 10 µg/mL and 20 µg/mL Propofol (Sigma-Aldrich) for 48 h. The control groups (0 µg/mL Propofol) were treated with the same volume of DMSO (Sigma-Aldrich) for 48 h.
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7

Propofol Modulates Tumor Growth in Nude Mice

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The female nude mice were obtained from Beijing Vital River Laboratory Animal Technology Co., Ltd. (Beijing, China) and divided into 6 groups (n=6/group): Model, Propofol, Propofol+vector, Propofol+oe-HOTAIR, Propofol+miR-NC and Propofol+miR-129-5p. The Model groups and Propofol groups were transplanted with HeLa cells (1×106 cells) and intraperitoneally injected with DMSO (DMSO; Sigma-Aldrich) or Propofol (35mg/kg; Sigma-Aldrich) every week for 4 continuous weeks after 10 days of HeLa cells injection. For Propofol+vector, Propofol+oe-HOTAIR, Propofol+miR-NC and Propofol+miR-129-5p groups, the mice were implanted with HeLa cells (1×106 cells) transfected with vector, oe-HOTAIR, miR-NC or miR-129-5p and intraperitoneally given Propofol (35mg/kg; Sigma-Aldrich) once per week for 4 continuous weeks. Tumor volume was monitored on days 5, 10, 17, 24, 31 and 38 and computed with the formula: (Length×width2)/2. On day 38, the mice were euthanized and tumor tissues were harvested and then weighed. The harvested tissues were saved at −80°C. The animal study was performed in accordance with the Guidelines for Care and Use of Laboratory Animals of “National Institutes of Health” and approved by the Ethics Committee of Animal Research of Zhengzhou Central Hospital Affiliated to Zhengzhou University.
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8

Synergistic Effects of Propofol and DDP on Ovarian Cancer

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DDP and propofol were purchased from Sigma-Aldrich; Merck KGaA. Different concentrations of propofol and DDP were used to treat ovarian cancer cell lines in a cell viability assay using different concentrations. For single agent treatment groups, ovarian cancer cells were treated with 0, 1, 5, 10 or 20 µg/ml propofol for 48 h at 37°C, or 0, 5, 10, 20 and 50 µM DDP for 48 h at 37°C. For the combined treatment group, A2780 or A2780/DDP cells were treated with 10 µg/ml propofol and 10 µM DDP for 48 h at 37°C. Cells were transfected with miR-374a or NC mimics before treatment with propofol and/or DDP.
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9

Endothelial Cell Injury Model with HCY and Propofol

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Human umbilical vein endothelial cells (HUVECs, PCS-100-010™) were purchased from the American Type Culture Collection, thawed at 37°C for 2 min, then transferred into a tube containing 5 ml RPMI-1640 medium (Gibco; Thermo Fisher Scientific, Inc.), followed by centrifugation at 1,000 × g and 4°C for 5 min. The supernatant was removed, then the cells were re-suspended in RPMI-1640 medium containing 100 U/ml penicillin, 100 µg/ml streptomycin and 10% FBS (Gibco; Thermo Fisher Scientific, Inc.). Subsequently, they were transferred into a 25-cm flask and incubated at 37°C in an humidified incubator with 5% CO2. The medium was replaced every 2 days. When the cells reached 80% confluence, they were washed with PBS twice, then 0.25% trypsin (1 ml) was added. After attachment, cells (70–80% confluence) were exposed to 2.5 mmol/l HCY (Sigma-Aldrich; Merck KGaA) at 37°C for 48 h to construct the endothelial cell injury model (2 (link)). For HCY and propofol (Sigma-Aldrich; Merck KGaA) co-treatment, adherent cells were pre-treated with indicated concentrations (12.5, 25, 50, 100 and 200 µM) of propofol at 37°C for 2 h, followed by exposure to 2.5 mmol/l HCY for 48 h. Untreated cells were used as the control group. Then, cells were collected for the following analysis.
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10

Preparation of Solutions for Neuroscience Experiments

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Salts used in ND96, HEPES, GABA, propofol, and 5β-pregnan-3α-ol-20-one (3α5βP) were purchased from Sigma-Aldrich (St. Louis, MO, USA). Etomidate was purchased from Toronto Research Chemicals (Toronto, ON, Canada). NS-1738 was obtained from Cayman Chemical (Ann Arbor, MI, USA) and Adooq Bioscience (Irvine, CA, USA). PAM-2 was synthesized as described previously [33 (link)]. A stock solution of 500 mM GABA in ND96 was stored at 4 °C. All other stock solutions were made in dimethyl sulfoxide (Sigma-Aldrich) with 200 mM propofol and 20 mM 3α5βP stocks stored at room temperature and 200 mM Etomidate, 100 mM NS-1738, and 100 mM PAM-2 stocks stored at −20 °C. Final dilutions were made on the day of the experiment.
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