The Neuroprotective Effects of Brazilian Green Propolis on Neurodegenerative Damage in Human Neuronal SH-SY5Y Cells.
Junjun NiZhou WuJie MengAiqin ZhuXin ZhongShizheng WuHiroshi NakanishiPublished in: Oxidative medicine and cellular longevity (2017)
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.
Keyphrases
- cell death
- cell cycle arrest
- oxidative stress
- induced apoptosis
- diabetic rats
- hydrogen peroxide
- mild cognitive impairment
- cognitive impairment
- endothelial cells
- high glucose
- reactive oxygen species
- poor prognosis
- dna damage
- cognitive decline
- endoplasmic reticulum stress
- ejection fraction
- drug induced
- transcription factor
- signaling pathway
- risk assessment
- brain injury
- spinal cord injury
- cell proliferation
- ischemia reperfusion injury
- high resolution
- cell free
- cerebral ischemia
- protein kinase
- heat shock protein
- human health