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Open Access Research article

Neuroprotective effects of melittin on hydrogen peroxide-induced apoptotic cell death in neuroblastoma SH-SY5Y cells

Sang Mi Han1*, Jung Min Kim1, Kwan Kyu Park2, Young Chae Chang2 and Sok Cheon Pak3

Author Affiliations

1 Department of Agricultural Biology, National Academy of Agricultural Science, RDA, Suwon 441-100, Korea

2 College of Medicine, Catholic University of Daegu, Daegu 712-702, Korea

3 School of Biomedical Sciences, Charles Sturt University, Bathurst NSW 2795, Australia

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BMC Complementary and Alternative Medicine 2014, 14:286  doi:10.1186/1472-6882-14-286

Published: 5 August 2014

Abstract

Background

Free radicals are involved in neuronal cell death in human neurodegenerative diseases. Since ancient times, honeybee venom has been used in a complementary medicine to treat various diseases and neurologic disorders. Melittin, the main component of honeybee venom, has various biologic effects, including anti-bacterial, anti-viral, and anti-inflammatory activities.

Methods

We investigated the neuroprotective effects of melittin against H2O2-induced apoptosis in the human neuroblastoma cell line SH-SY5Y. The neuroprotective effects of melittin on H2O2-induced apoptosis were investigated using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenylterazolium bromide assay, caspase 3 activity, 4,6-diamidino-2-phenylindole staining, a lactate dehydrogenase release assay, Western blots, and reverse transcription-polymerase chain reaction.

Results

The H2O2-treated cells had decreased cell viability with apoptotic features and increased production of caspase-3. On the other hand, melittin treatment increased cell viability and decreased apoptotic DNA fragmentation. Melittin attenuated the H2O2-induced decrease in mRNA and protein production of the anti-apoptotic factor Bcl-2. In addition, melittin inhibited both the H2O2-induced mRNA and protein expression of Bax-associated pro-apoptotic factor and caspase-3.

Conclusions

These findings suggest that melittin has potential therapeutic effects as an agent for the prevention of neurodegenerative diseases.