Abstract
Oxidative stress and synapse dysfunction are the major neurodegenerative damage correlated to cognitive impairment in Alzheimer's disease (AD). We have found that Brazilian green propolis (propolis) improves the cognitive functions of mild cognitive impairment patients living at high altitude; however, mechanism underlying the effects of propolis is unknown. In the present study, we investigated the effects of propolis on oxidative stress, expression of brain-derived neurotrophic factor (BDNF), and activity-regulated cytoskeleton-associated protein (Arc), the critical factors of synapse efficacy, using human neuroblastoma SH-SY5Y cells. Pretreatment with propolis significantly ameliorated the hydrogen peroxide- (H2O2-) induced cytotoxicity in SH-SY5Y cells. Furthermore, propolis significantly reduced the H2O2-generated reactive oxygen species (ROS) derived from mitochondria and 8-oxo-2′-deoxyguanosine (8-oxo-dG, the DNA oxidative damage marker) but significantly reversed the fibrillar β-amyloid and IL-1β-impaired BDNF-induced Arc expression in SH-SY5Y cells. Furthermore, propolis significantly upregulated BDNF mRNA expression in time- and dose-dependent manners. In addition, propolis induced Arc mRNA and protein expression via phosphoinositide-3 kinase (PI3K). These observations strongly suggest that propolis protects from the neurodegenerative damage in neurons through the properties of various antioxidants. The present study provides a potential molecular mechanism of Brazilian green propolis in prevention of cognitive impairment in AD as well as aging.
Highlights
Alzheimer’s disease (AD) is the most common form of dementia in aging societies worldwide [1] and the number of AD is growing dramatically [2]
We focused on the effects of propolis on the hydrogen peroxide- (H2O2) induced oxidative stress, and expression of brain-derived neurotrophic factor (BDNF) and Arc using cultured human neuroblastoma SH-SY5Y cells, which are widely used for the study of neurodegenerative damage in vitro [36]
We examined the effects of propolis on BDNF expression in SH-SY5Y cells, because BDNF is the critical neurotrophic factor that is important for synapse efficacy
Summary
Alzheimer’s disease (AD) is the most common form of dementia in aging societies worldwide [1] and the number of AD is growing dramatically [2]. Activity-regulated cytoskeleton-associated protein (Arc) is a critical immediate-early gene that has been implicated in generated stable changes in synaptic efficacy [14, 15], as suppression of Arc expression impairs the synaptic plasticity and memory consolidation [11, 14, 16]. Fibrillar β-amyloid, the main component of plaques in the brains of AD patients, has been shown to impair the BDNF-induced Arc expression in the cultured cortical neurons, even at low levels [21]; interfering with BDNF signaling affects the downstream neuronal functions that contribute to the development of AD [22].
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