Taurine (2-aminoethanesulfonic acid) is a non-protein β-amino acid essential for cellular homeostasis, with antioxidant, anti-inflammatory, and cytoprotective properties that are crucial for life maintenance. This study aimed to evaluate the effects of taurine administration on hippocampal neurogenesis, neuronal preservation, or reverse damage in rats exposed to forced ethanol consumption in an animal model. Wistar rats were treated with ethanol (EtOH) for a 28-day period (5% in the 1st week, 10% in the 2nd week, and 20% in the 3rd and 4th weeks). Two taurine treatment protocols (300 mg/kg i.p.) were implemented: one during ethanol consumption to analyze neuroprotection, and another after ethanol consumption to assess the reversal of ethanol-induced damage. Overall, the results demonstrated that taurine treatment was effective in protecting against deficits induced by ethanol consumption in the dentate gyrus. The EtOH+TAU group showed a significant increase in cell proliferation (145.8%) and cell survival (54.0%) compared to the EtOH+Sal group. The results also indicated similar effects regarding the reversal of ethanol-induced damage 28 days after the cessation of ethanol consumption. The EtOH+TAU group exhibited a significant increase (41.3%) in the number of DCX-immunoreactive cells compared to the EtOH+Sal group. However, this amino acid did not induce neurogenesis in the tissues of healthy rats, implying that its activity may be contingent upon post-injury stimuli.
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http://dx.doi.org/10.3390/nu16121973 | DOI Listing |
BMC Chem
January 2025
Department of Pharmaceutical Analytical Chemistry, Faculty of Pharmacy, University of Alexandria, Elmessalah, Alexandria, 21521, Egypt.
A simple, rapid, and reproducible high-performance liquid chromatography (HPLC) method has been developed and validated for the determination of β-sitosterol in the pharmaceutical dosage form of moist exposed burn ointment (MEBO). This method involved an effective sample procedure for extraction of β-sitosterol from MEBO using an alkali saponification agent composed of 0.8 N ethanolic NaOH and diethyl ether.
View Article and Find Full Text PDFFree Radic Biol Med
January 2025
Department of Forensic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China. Electronic address:
Chronic ethanol (EtOH) consumption has been widely recognized as a significant contributor to cardiotoxicity. However, no specific treatment is currently available to ameliorate chronic ethanol induced cardiotoxicity. Adiponectin receptor agonist AdipoRon exerts protective effects in multiple organs through alleviating lipotoxicity.
View Article and Find Full Text PDFBioresour Technol
January 2025
Department of Biology, University of Padova, 35131 Padova, Italy. Electronic address:
The fermentation process in alcoholic beverage production converts sugars into ethanol and CO, releasing significant amounts of greenhouse gases. Here, Cupriavidus necator DSM 545 was grown autotrophically using gas derived from alcoholic fermentation, using a fed-batch bottle system. Nutrient starvation was applied to induce intracellular accumulation of poly(3-hydroxybutyrate) (PHB), a bioplastic polymer, for bioconversion of CO-rich waste gas into PHB.
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January 2025
College of Life Sciences, Institute of Life Science and Green Development, Hebei University, Baoding 071002, China; The Key Laboratory of Zoological Systematics and Application, College of Life Sciences, Hebei University, Baoding 071002, China. Electronic address:
Excessive alcohol consumption is a major cause of alcoholic cardiomyopathy (ACM) and myocardial injury. This study aims to investigate the role of transcription factor EB (TFEB) in ethanol-induced cardiac anomalies using a murine model, AC16 human cardiomyocytes, and human plasma. Wild-type mice treated with a TFEB activator (Compound 1) or vehicle (25 mg/kg/d) were challenged with or without ethanol (3 g/kg/d, i.
View Article and Find Full Text PDFJ Physiol
January 2025
Department of Internal and Experimental Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Important health disparities are observed in the prevalence of obesity and associated non-communicable diseases (NCDs), including type 2 diabetes (T2D) and metabolic dysfunction-associated steatotic liver disease (MASLD) among ethnic groups. Yet, the underlying factors accounting for these disparities remain poorly understood. Fructose has been widely proposed as a potential mediator of these NCDs, given that hepatic fructose catabolism can result in deleterious metabolic effects, including insulin resistance and hepatic steatosis.
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