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Remimazolam Suppresses Oxidative Stress and Apoptosis in Cerebral Ischemia/Reperfusion Injury by Regulating AKT/GSK-3β/NRF2 Pathway.
Drug Des Devel Ther
January 2025
Department of Anesthesiology, The Affiliated Hospital of Qingdao University, Qingdao, People's Republic of China.
Introduction: The mechanism of remimazolam, a benzodiazepine that activates γ-aminobutyric acid a (GABAa) receptors, in cerebral ischemia/reperfusion (I/R) injury is not well understood. Therefore, we explored whether remimazolam activates protein kinase B (AKT)/glycogen synthase kinase-3β (GSK-3β)/nuclear factor erythroid 2-related factor 2 (NRF2) to attenuate brain I/R injury in transcerebral I/R-injured rats and transoxygenic glucose deprivation/reperfusion (OGD/R)-injured SY5Y cells.
Material And Methods: Remimazolam was added at the beginning of cell and rat reperfusion, and the PI3K/AKT inhibitor LY294002 was added to inhibit the AKT/GSK-3β/NRF2 pathway 24 h before cellular OGD/R treatment and 30 min before rat brain I/R treatment.
[Berberine regulates glucose and lipid metabolism via clock-controlled genes to ameliorate insulin resistance of hepatocytes].
Zhongguo Zhong Yao Za Zhi
December 2024
Jiangxi Province Key Laboratory of Traditional Chinese Medicine Etiopathogenisis & Research Center for Differentiation and Development of Traditional Chinese Medicine Basic Theory, Jiangxi University of Chinese Medicine Nanchang 330004,China.
This study aims to investigate the mechanism of berberine in regulating the metabolism network via clock-controlled genes represented by brain and muscle arnt-like 1(BMAL1) to ameliorate insulin resistance(IR) of hepatocytes in vitro. The HepG2 cell model of dexamethasone-induced IR(IR-HepG2) was established and treated with 5, 10, and 20 μmol·L~(-1) berberine, respectively, for 24 h. The glucose oxidase method and cell counting kit-8(CCK-8) assay were employed to measure extracellular glucose concentration and cell viability, respectively.
View Article and Find Full Text PDFPhenylbutyric Acid Modulates Apoptosis and ER Stress-Related Gene Expression in Glycogen Storage Disease Type Ib In Vitro Model.
Mol Genet Genomic Med
January 2025
Group for Rare Disease Research and Therapeutics Development, Institute of Molecular Genetics and Genetic Engineering, University of Belgrade, Belgrade, Republic of Serbia.
Introduction: Chronic endoplasmic reticulum (ER) stress and increased apoptosis are involved in the pathogenesis of glycogen storage disease Ib (GSD Ib), whereas small molecule phenylbutyrate (4-PBA) showed the capability of reducing ER stress-induced apoptosis. The objective was to generate an in vitro system in which capability of small molecules (SMs) to influence ER stress and apoptosis could be screened at the expression level.
Methods: G6PT-deficient FlpInHEK293 cell line was created and validated using the CRISPR/Cas9 knockout method.
In depth profiling of dihydrolipoamide dehydrogenase deficiency in primary patients fibroblasts reveals metabolic reprogramming secondary to mitochondrial dysfunction.
Mol Genet Metab Rep
March 2025
The Shmunis School of Biomedicine and Cancer Research, The George S. Wise Faculty for Life Sciences, Sagol School of Neurosciences, Tel Aviv University, 6997801 Tel Aviv, Israel.
Dihydrolipoamide dehydrogenase (DLD) deficiency is an autosomal recessive disorder characterized by a functional disruption in several critical mitochondrial enzyme complexes, including pyruvate dehydrogenase and α-ketoglutarate dehydrogenase. Despite DLD's pivotal role in cellular energy metabolism, detailed molecular and metabolic consequences of DLD deficiency (DLDD) remain poorly understood. This study represents the first in-depth multi-omics analysis, specifically metabolomic and transcriptomic, of fibroblasts derived from a DLD-deficient patient compound heterozygous for a common Ashkenazi Jewish variant (c.
View Article and Find Full Text PDFChronic bacterial infections exert metabolic costs in Drosophila melanogaster.
J Exp Biol
January 2025
Department of Entomology, Cornell University, Ithaca, NY 14853, USA.
Bacterial infections can substantially impact host metabolic health as a result of the direct and indirect demands of sustaining an immune response and of nutrient piracy by the pathogen itself. Drosophila melanogaster and other insects that survive a sublethal bacterial infection often carry substantial pathogen burdens for the remainder of life. In this study, we asked whether these chronic infections exact metabolic costs for the host, and how these costs scale with the severity of chronic infection.
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