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Propofol is the most widely accepted intravenous anesthetic available for clinical use. However, neurotoxicity of propofol in the developing brain has been reported. This study investigated the effects of propofol on cognitive function in normal healthy adult mice. Thirty-three GFP-LC3 adult mice were included. Propofol was injected for anesthesia (n = 22). The sham control (n = 11) received intralipid injections. The mice completed a Y-maze test on 3 and 7 days after being anesthetized. Western blotting, immunofluorescence staining, and transmission electron microscopic (TEM) analyses were performed with their hippocampi. In addition, we conducted a separate ex vivo experiment using organotypic hippocampal slice cultures (OHSCs) to investigate the effects of propofol on induced autophagy. There was a significantly lower percentage of alternation in the Y-maze test on day 3 after propofol anesthesia than the control, but no difference was observed on day 7. Western blot analyses and immunofluorescence assays showed that the levels of cognitive function-related proteins significantly decreased in the propofol group compared to the control on day 3 but had recovered by day 7. In terms of autophagy-related proteins, western blot analyses and immunofluorescence assays showed that propofol increased autophagic induction, flux, and degradation of autophagosomes. Ex vivo experiments showed that propofol enhanced autophagic flux of the induced autophagy. In conclusion, although transient cognitive dysfunction occurred, adult mice recovered their cognitive function after the administration of propofol anesthesia. And this finding may be associated with enhanced autophagic flux.
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http://dx.doi.org/10.1016/j.brainres.2018.07.007 | DOI Listing |
JCI Insight
September 2025
Diabetes & Metabolism Research Center, University of Utah, Salt Lake City, United States of America.
Impaired muscle regrowth in aging is underpinned by reduced pro-inflammatory macrophage function and subsequently impaired muscle cellular remodeling. Macrophage phenotype is metabolically controlled through TCA intermediate accumulation and activation of HIF1A. We hypothesized that transient hypoxia following disuse in old mice would enhance macrophage metabolic inflammatory function thereby improving muscle cellular remodeling and recovery.
View Article and Find Full Text PDFMetabolomics
September 2025
Department of Biochemistry, University of Oxford, South Parks Road, Oxford, OX1 3QU, UK.
Introduction: Knockout of the Fmo5 gene in mice led to a lean, slow-ageing phenotype characterised by the presence of 2,3-butanediol isomers in their urine and plasma. Oral treatment of wildtype mice with 2,3-butanediol led to a low cholesterol, low epididymal fat phenotype.
Objectives: Determine if significant, heterozygous coding variations in human FMO5 would give rise to similar clinical and metabolic phenotypes in humans, as in C57BL/6J mice with knockout of the Fmo5 gene and in particular, increased excretion of 2,3-butanediol.
Acta Parasitol
September 2025
Department of Zoology, B. Borooah College, Guwahati, Assam, 781007, India.
Background: The whole plant of Evolvulus nummularius is traditionally used to treat helminth infections in Assam, India. This study was taken to evaluate the efficacy of its methanolic extract in suitable models in vitro and in vivo.
Methods: Hymenolepis diminuta exposed in vitro to E.
World J Urol
September 2025
Department of Pharmacology, Faculty of Medical Sciences, University of Campinas (UNICAMP), Campinas, Sao Paulo, Brazil.
Purpose: To evaluate the impact of MRP inhibition by MK571 on prostate hypercontractility in diet-induced obesity, based on the hypothesis that this intervention enhances intracellular cAMP and cGMP signaling.
Methods: Adult C57BL/6 mice were divided into three groups: (i) lean, (ii) obese, and (iii) obese + MK571 (5 mg/kg/day, 14 days). The prostate was isolated for immunohistochemistry, biochemistry and functional assays.
Elife
September 2025
Department of Neuroscience, Washington University School of Medicine, St Louis, United States.
Peripheral sensory neurons regenerate their axons after injury to regain function, but this ability declines with age. The mechanisms behind this decline are not fully understood. While excessive production of endothelin 1 (ET-1), a potent vasoconstrictor, is linked to many diseases that increase with age, the role of ET-1 and its receptors in axon regeneration is unknown.
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