期刊论文详细信息
BMC Complementary and Alternative Medicine
Edible bird’s nest ameliorates oxidative stress-induced apoptosis in SH-SY5Y human neuroblastoma cells
Khuen Yen Ng2  Iekhsan Othman2  Soi Moi Chye1  Rhun Yian Koh1  Mei Yeng Yew2 
[1] Department of Human Biology, School of Medicine, International Medical University, Kuala Lumpur, Malaysia;Jeffrey Cheah School of Medicine & Health Sciences, Monash University Malaysia, Selangor, Malaysia
关键词: Neuroprotection;    Parkinson’s disease;    Neurodegenerative disorder;    6-OHDA;    SH-SY5Y;    Apoptosis;    Edible bird’s nest;   
Others  :  1086104
DOI  :  10.1186/1472-6882-14-391
 received in 2014-04-25, accepted in 2014-10-01,  发布年份 2014
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【 摘 要 】

Background

Parkinson’s disease (PD) is the second most common neurodegenerative disorder affecting the senile population with manifestation of motor disability and cognitive impairment. Reactive oxygen species (ROS) is implicated in the progression of oxidative stress-related apoptosis and cell death of the midbrain dopaminergic neurons. Its interplay with mitochondrial functionality constitutes an important aspect of neuronal survival in the perspective of PD. Edible bird’s nest (EBN) is an animal-derived natural food product made of saliva secreted by swiftlets from the Aerodamus genus. It contains bioactive compounds which might confer neuroprotective effects to the neurons. Hence this study aims to investigate the neuroprotective effect of EBN extracts in the neurotoxin-induced in vitro PD model.

Methods

EBN was first prepared into pancreatin-digested crude extract and water extract. In vitro PD model was generated by exposing SH-SY5Y cells to neurotoxin 6-hydroxydopamine (6-OHDA). Cytotoxicity of the extracts on SH-SY5Y cells was tested using MTT assay. Then, microscopic morphological and nuclear examination, cell viability test and ROS assay were performed to assess the protective effect of EBN extracts against 6-OHDA-induced cellular injury. Apoptotic event was later analysed with Annexin V-propidium iodide flow cytometry. To understand whether the mechanism underlying the neuroprotective effect of EBN was mediated via mitochondrial or caspase-dependent pathway, mitochondrial membrane potential (MMP) measurement and caspase-3 quantification were carried out.

Results

Cytotoxicity results showed that crude EBN extract did not cause SH-SY5Y cell death at concentrations up to 75 μg/ml while the maximum non-toxic dose (MNTD) of water extract was double of that of crude extract. Morphological observation and nuclear staining suggested that EBN treatment reduced the level of 6-OHDA-induced apoptotic changes in SH-SY5Y cells. MTT study further confirmed that cell viability was better improved with crude EBN extract. However, water extract exhibited higher efficacy in ameliorating ROS build up, early apoptotic membrane phosphatidylserine externalization as well as inhibition of caspase-3 cleavage. None of the EBN treatment had any effect on MMP.

Conclusions

Current findings suggest that EBN extracts might confer neuroprotective effect against 6-OHDA-induced degeneration of dopaminergic neurons, particularly through inhibition of apoptosis. Thus EBN may be a viable nutraceutical option to protect against oxidative stress-related neurodegenerative disorders such as PD.

【 授权许可】

   
2014 Yew et al.; licensee BioMed Central Ltd.

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