Background: Chronic excessive ethanol consumption damages the central nervous system and causes neurobehavioral changes, such as cognitive impairment, which is related to oxidative stress and inhibition of neurogenesis in the hippocampus. It is known that promoting neurogenesis improves learning memory, anxiety and depression. Lycium barbarum L. polyphenol (LBP) is the main active ingredient of Lycium barbarum L., which has excellent neuroprotective effects. However, the effects and mechanisms of LBP on ethanol-induced cognitive impairment are unclear.
Purpose: To assess the effects and mechanisms of LBP on ethanol-induced cognitive impairment in mice.
Methods: Eight-weeks-old adult C57BL/6J mice were allowed to drink ethanol (10%) to establish a model of ethanol-induced cognitive impairment. From the 29th day of LBP (25, 50, 100, 200, 400 mg/kg, intragastric administration), the locomotor activity, novel object recognition (NOR), Y maze and Morris water maze (MWM) were sequentially performed to investigate the effect of LBP on ethanol-induced cognitive impairment in mice. Next, enzyme-linked immunosorbent assay, immunofluorescence, and western blotting were used to study the underlying mechanism of LBP on ethanol-induced cognitive impairment.
Results: LBP significantly decreased the escape latency and increased the number of crossings of the original platform in MWM, increased the spontaneous alteration behavior in the Y maze, and increased the preference index in the NOR in ethanol-induced mice. Notably, LBP significantly promoted the proliferation of neural stem cells, neural progenitor cells and neuroblasts, and increased the proportion of activated NSCs in mice with ethanol-induced cognitive impairment. Similarly, LBP significantly increased the number of newborn immature neurons and mature neurons. Moreover, LBP increased the levels of nuclear factor erythroid2-related factor 2 (Nrf2) and the downstream heme oxygenase-1(HO-1) protein expression, which led to a decrease of oxidative stress levels.
Conclusion: LBP significantly improves cognitive impairment in ethanol-induced mice, which is attributed to the promotion of hippocampal neurogenesis and reduction of oxidative stress.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.phymed.2022.154033 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Long-Term Intake of Red Meat in Relation to Dementia Risk and Cognitive Function in US Adults.
Neurology
February 2025
Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA.
Background And Objectives: Previous studies have shown inconsistent associations between red meat intake and cognitive health. Our objective was to examine the association between red meat intake and multiple cognitive outcomes.
Methods: In this prospective cohort study, we included participants free of dementia at baseline from 2 nationwide cohort studies in the United States: the Nurses' Health Study (NHS) and the Health Professionals Follow-Up Study (HPFS).
Morbidity and factors associated with frailty in post-COVID-19 elderly patients attended at a reference center.
Rev Bras Enferm
January 2025
Universidade Estadual de Montes Claros. Montes Claros, Minas Gerais, Brazil.
Objective: To assess the morbidity profile and identify factors associated with frailty syndrome in post-COVID-19 elderly patients treated at the only Reference Center for Elderly Health Care in northern Minas Gerais.
Methods: This is a case series study, utilizing the Clinical-Functional Vulnerability Index-20 (CFVI-20) and Comprehensive Geriatric Assessment (CGA) to characterize and evaluate the health condition of the group. To define the variables associated with frailty, a multivariate analysis was conducted.
Effects of Tesamorelin on Neurocognitive Impairment in Abdominally Obese Persons with HIV.
J Infect Dis
January 2025
Department of Internal Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Background: In people with HIV (PWH) who are virally suppressed (VS) on antiretroviral therapy (ART), abdominal obesity (AO) is linked to neurocognitive impairment (NCI), potentially due to visceral adiposity, inflammation, and reduced insulin-like growth factor 1 (IGF-1). Tesamorelin, a growth hormone-releasing hormone, reduces AO and increases IGF-1, suggesting it might mitigate NCI in VS PWH.
Methods: This 6-month, Phase II randomized, open-label clinical trial compared Tesamorelin versus standard-of-care (SOC) for NCI in abdominally obese PWH.
Senescence Accelerated Mouse-Prone 8: a Model of Neuroinflammation and Aging with Features of Sporadic Alzheimer's disease.
Stem Cells
January 2025
Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX13QX, UK.
The large majority of Alzheimer's disease (AD) cases are sporadic with unknown genetic causes. In contrast, only a small percentage of AD cases are familial, with known genetic causes. Paradoxically, there are only few validated mouse models of sporadic AD but many of familial AD.
View Article and Find Full Text PDFAnterior-temporal network hyperconnectivity is key to Alzheimer's disease: from ageing to dementia.
Brain
January 2025
U1237, Physiopathology and Imaging of Neurological Disorders (PhIND), Neuropresage Team; INSERM, University of Caen Normandy; GIP Cyceron, 14000 Caen, France.
Curing Alzheimer's disease remains hampered by an incomplete understanding of its pathophysiology and progression. Exploring dysfunction in medial temporal lobe networks, particularly the anterior-temporal (AT) and posterior-medial (PM) systems, may provide key insights, as these networks exhibit functional connectivity alterations along the entire Alzheimer's continuum, potentially influencing disease propagation. However, the specific changes in each network and their clinical relevance across stages are not yet fully understood.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!