Abstract
Neurodegenerative diseases remain a significant unresolved societal burden afflicting millions of people worldwide. Neurons in the brain are highly sensitive to oxidative stress, which can be induced by metal toxicity. In this paper, a chronic aluminum overload-induced model of neurodegeneration was used to investigate whether metal ions (Al, Fe, Mn, Cu and Zn)-related oxidative stress was involved in neurodegenerative mechanism and to identify the protective action of meloxicam against rat hippocampal neuronal injury. The metal ion contents, activity of superoxide dismutase (SOD), and content of malondialdehyde (MDA) were detected. The results showed that the spatial learning and memory (SLM) function was significantly impaired in chronic aluminum overload rats. Considerable karyopycnosis was observed in hippocampal neurons. The SOD activity was weakened and the MDA content increased both significantly. In the hippocampus, Al, Fe, Mn, Cu, and Zn contents increased by 184.1%, 186.1%, 884.2%, 199.4% and 149.2%, respectively. Meloxicam administration (without Al) had no effect compared with the control group, while meloxicam treatment with aluminum exposure significantly protected rats from SLM function impairment, neuron death, lower SOD activity, higher MDA content and brain metal ion imbalance. Our findings suggest that the cerebral metal ion imbalance-related oxidative stress is involved in mechanism of cerebral injury and neurodegeneration induced by chronic Al overload in rats, and that meloxicam protects neurons by reducing metal ion imbalance-related oxidative stress.
Highlights
Neurodegenerative diseases (NDDs), including Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), Amyotrophic lateral sclerosis (ALS), Spinal muscular atrophy (SMA) and related neurological and psychiatric disorders, encompass a group of neurological disorders
The aim of this study is to reveal whether the protective mechanism of meloxicam against rat hippocampal neuronal injury involves the reduction of the metal ion imbalance and oxidative stress
Metal ions are required for maintaining the functions of many proteins and proper metal ion balance in the brain is significant for normal cognitive function [22]
Summary
Neurodegenerative diseases (NDDs), including Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), Amyotrophic lateral sclerosis (ALS), Spinal muscular atrophy (SMA) and related neurological and psychiatric disorders, encompass a group of neurological disorders. Neurodegeneration can be described as loss of neuronal structure and function, and is manifested as loss of memory, cognition, movement or its control, and sensation [1]. AD is characterized by memory loss and cognitive impairment [2], PD can cause cognitive impairment, including dementia and behavioral changes [3], and HD is manifested with dementia, involuntary motor activity, NDDs are progressive, with reflective of increased neuron death. The major mechanisms in pathogenic processes of NDDs include oxidative stress, protein aggregation, inflammation, blood brain barrier (BBB) disruption, and mitochondrial dysfunction. Oxidative stress is one major molecular mechanism responsible for the pathogenesis and progression of several NDDs [5]. Oxidative damage and mitochondrial dysfunction have been described in patients with AD, PD, HD, and ALS [6,7]. Much research on neurodegeneration is fragmentary, leaving the mechanisms of NDDs unresolved
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