AI Article Synopsis
Article Abstract
Background: alpha-Mangostin, a polyphenolic xanthone, is primarily found in the pericarp of mangosteen throughout Southeast Asia and is considered as the "Queen of Fruit" in Thailand. Nonetheless, it is not clarified how alpha-mangostin protects neuronal cells against oxidative stress.
Objective: In this study, molecular mechanisms underlying the neuroprotective effect of alpha-mangostin in defending hydrogen peroxide (HO)-induced neurotoxicity was explored.
Methods: cytotoxicity, reactive oxygen species (ROS) generation, apoptotic cascades, and protein expression profiles were performed incorporation of molecular docking.
Results: Human SH-SY5Y cells were pretreated with 1 μM alpha-mangostin for 3 h prior to exposure to 400 μM HO. alpha-Mangostin significantly inhibited oxidative stress-induced cell death in neuronal cells by reducing BAX protein, decreasing caspase-3/7 activation, and increasing anti-apoptotic BCL-2 protein. Collectively, alpha-mangostin was demonstrated to be a prominent ROS suppressor which reversed the reduction of antioxidant enzymes (CAT and SOD2). Surprisingly, alpha-mangostin significantly promoted the expression of the sirtuin family and the FOXO3a transcription factor exerting beneficial effects on cell survival and longevity. A molecular docking study predicted that alpha-mangostin is directly bound to the active site of SIRT1.
Conclusion: Findings from this study suggest that alpha-mangostin potentially serves as a promising therapeutic compound against oxidative stress by activation of the SIRT1/3-FOXO3a pathway comparable to the effect of memantine, an anti-AD drug used for the treatment of moderate to severe dementia.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8835347 | PMC |
| http://dx.doi.org/10.3389/fnut.2021.714463 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Intrinsic Muscle Stem Cell Dysfunction Contributes to Impaired Regeneration in the mdx Mouse.
J Cachexia Sarcopenia Muscle
February 2025
Sprott Centre for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Canada.
Background: Duchenne muscular dystrophy (DMD) is a devastating disease characterized by progressive muscle wasting that leads to diminished lifespan. In addition to the inherent weakness of dystrophin-deficient muscle, the dysfunction of resident muscle stem cells (MuSC) significantly contributes to disease progression.
Methods: Using the mdx mouse model of DMD, we performed an in-depth characterization of disease progression and MuSC function in dystrophin-deficient skeletal muscle using immunohistology, isometric force measurements, transcriptomic analysis and transplantation assays.
Gender Differences in Dendritic Damage, Gut Microbiota Dysbiosis, and Cognitive Impairment During Aging Processes.
CNS Neurosci Ther
December 2024
Department of Radiology, The Affiliated Panyu Central Hospital of Guangzhou Medical University, Guangzhou, China.
Background: Cognitive impairment is a common and feared characteristic of aging processes, and one key mechanism of cognition is hippocampal synaptic structure. Previous studies have reported that gut microbiota dysbiosis occurred in neurodegenerative diseases and other brain disorders with cognitive impairment. However, it is not clear how gender differences affect cognitive impairment in aging processes and whether they affect synaptic structure and gut microbiota.
View Article and Find Full Text PDFTargeting Remyelination in Spinal Cord Injury: Insights and Emerging Therapeutic Strategies.
CNS Neurosci Ther
December 2024
Central Laboratory of The Lishui Hospital of Wenzhou Medical University, The First Affiliated Hospital of Lishui University, Lishui People's Hospital, Lishui, Zhejiang, China.
Introduction: Spinal cord injury (SCI) is a severe neurological disease characterized by significant motor, sensory, and autonomic dysfunctions. SCI is a major global disability cause, often resulting in long-term neurological impairments due to the impeded regeneration and remyelination of axons. A SCI interferes with communication between the brain and the spinal cord networks that control neurological functions.
View Article and Find Full Text PDFPathological mechanisms of glial cell activation and neurodegenerative and neuropsychiatric disorders caused by infection.
Front Microbiol
December 2024
Department of Pathogen Biology, Guangdong Provincial Key Laboratory of Tropical Diseases Research, School of Public Health, Key Laboratory of Infectious Diseases Research in South China (Southern Medical University), Ministry of Education, Southern Medical University, Guangzhou, Guangdong, China.
is an intracellular opportunistic parasite that exists in a latent form within the human central nervous system (CNS), even in immune-competent hosts. During acute infection, traverses the blood-brain barrier (BBB). In the subsequent chronic infection phase, the infiltration of immune cells into the brain, driven by infection and the formation of parasitic cysts, leads to persistent activation and proliferation of astrocytes and microglia.
View Article and Find Full Text PDFGeneration and characterization of two induced pluripotent stem cell lines (ICGi052-A and ICGi052-B) from a patient with frontotemporal dementia with parkinsonism-17 associated with the pathological variant c.2013T>G in the MAPT gene.
Vavilovskii Zhurnal Genet Selektsii
November 2024
Institute of Cytology and Genetics of the Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russia Institute of Chemical Biology and Fundamental Medicine of the Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russia.
Frontotemporal dementia with parkinsonism-17 is a neurodegenerative disease characterised by pathological aggregation of the tau protein with the formation of neurofibrillary tangles and subsequent neuronal death. The inherited form of frontotemporal dementia can be caused by mutations in several genes, including the MAPT gene on chromosome 17, which encodes the tau protein. As there are currently no medically approved treatments for frontotemporal dementia, there is an urgent need for research using in vitro cell models to understand the molecular genetic mechanisms that lead to the development of the disease, to identify targets for therapeutic intervention and to test potential drugs to prevent neuronal death.
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!