Background: Alcohol-induced cerebellar neurodegeneration is a neuroadaptation that is associated with chronic alcohol abuse. Conventional drugs have been largely unsatisfactory in preventing neurodegeneration. Yet, multimodal neuro-protective therapeutic agents have been hypothesised to have high therapeutic potential for the treatment of CNS conditions; there is yet a dilemma of how this would be achieved. Contrarily, medicinal botanicals are naturally multimodal in their mechanism of action.
Aim: The effect of L. owariensis was therefore assessed in alcohol-induced neurodegeneration of the cerebellar cortex in rats.
Materials And Methods: Two groups of rats were oro-gastrically fed thrice daily with 5 g/kg ethanol (25% w/v), and 5 g/kg ethanol (25% w/v) plus L. owariensis (100 mg/kg body weight) respectively in diluted nutritionally complete diet (50% v/v). A control group was correspondingly fed a nutritionally complete diet (50% v/v) made isocaloric with glucose. Cytoarchitectural study of the cerebellar cortex was examined with H&E. Immunocytochemical analysis was carried out with the use of monoclonal antibody anti-NF in order to detect alterations in the neuronal cytoskeleton.
Results: After 4 days of binge alcohol treatment, we observed that L. owariensis supplementation significantly lowered the levels of histologic and biochemical indices of neurodegeneration. The level of neurodegeneration and cytoarchitecture distortion of the cerebellar cortex of rats exposed to ethanol was reduced by L. owariensis. Neurofilament-immunoreactivity (NF-IR) was evoked in the Purkinje cells of rats that received L. owariensis supplement.
Conclusions: L. owariensis attenuates alcohol-induced cerebellar degeneration in the rat by alleviating oxidative stress and alteration of NF protein expression in the Purkinje cells.
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http://dx.doi.org/10.1515/folmed-2016-0034 | DOI Listing |
Front Cell Dev Biol
February 2024
Department of Medicine, Division of Gastroenterology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, United States.
Granulocyte colony-stimulating factor (G-CSF) has been proposed as a therapeutic option for patients with ACLF, however clinical outcomes are controversial. We aimed at dissecting the role of G-CSF in an alcohol-induced murine model of ACLF. : ACLF was triggered by a single alcohol binge (5 g/kg) in a bile duct ligation (BDL) liver fibrosis model.
View Article and Find Full Text PDFNeuropharmacology
May 2023
Animal Models Core Facility, The Scripps Research Institute, La Jolla, CA, 92037, USA.
Front Neurol
October 2022
Department of Neurology, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an, China.
Although numerous adverse effects of alcohol addiction on health, behavior, and brain function were widely reported, the neurobiological mechanism of alcohol dependence remains largely unknown. In this study, a total of twenty-nine patients with alcohol dependence and twenty-nine status-matched normal controls (NCs) were recruited. Percent amplitude of fluctuation (PerAF) was applied to identify alcohol-related brain activity deficits.
View Article and Find Full Text PDFFront Pharmacol
September 2022
Department of Psychobiology and Methods in Behavioral Science, Faculty of Psychology, Complutense University of Madrid, Madrid, Spain.
Wernicke's encephalopathy (WE) is a neurologic disease caused by vitamin B1 or thiamine deficiency (TD), being the alcohol use disorder its main risk factor. WE patients present limiting motor, cognitive, and emotional alterations related to a selective cerebral vulnerability. Neuroinflammation has been proposed to be one of the phenomena that contribute to brain damage.
View Article and Find Full Text PDFAlcohol
December 2022
Department of Pharmacology, Amity Institute of Pharmacy, Amity University Uttar Pradesh, Noida, India. Electronic address:
Prenatal alcohol exposure (PAE) has been shown to induce symptomatology associated with attention deficit hyperactivity disorder (ADHD) by altering neurodevelopmental trajectories. Phosphodiesterase-1 (PDE1) is expressed centrally and has been used in various experimental brain conditions. We investigated the role of vinpocetine, a PDE1 inhibitor, on behavioral phenotypes and important biochemical deficits associated with a PAE rat model of ADHD.
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