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Toxins 2015, 7(9), 3715-3726; doi:10.3390/toxins7093715

Bee Venom Protects against Rotenone-Induced Cell Death in NSC34 Motor Neuron Cells

1
Department of Medical Research, Korea Institute of Oriental Medicine, 483 Expo-ro, Yuseong-gu, Daejeon 305-811, Korea
2
Executive Director of R&D, Korea Institute of Oriental Medicine, 483 Expo-ro, Yuseong-gu, Daejeon 305-811, Korea
3
Department of Clinical Research, Korea Institute of Oriental Medicine, 483 Expo-ro, Yuseong-gu, Daejeon 305-811, Korea
*
Author to whom correspondence should be addressed.
Academic Editor: Ren Lai
Received: 8 July 2015 / Revised: 20 August 2015 / Accepted: 31 August 2015 / Published: 21 September 2015
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Abstract

Rotenone, an inhibitor of mitochondrial complex I of the mitochondrial respiratory chain, is known to elevate mitochondrial reactive oxygen species and induce apoptosis via activation of the caspase-3 pathway. Bee venom (BV) extracted from honey bees has been widely used in oriental medicine and contains melittin, apamin, adolapin, mast cell-degranulating peptide, and phospholipase A2. In this study, we tested the effects of BV on neuronal cell death by examining rotenone-induced mitochondrial dysfunction. NSC34 motor neuron cells were pretreated with 2.5 μg/mL BV and stimulated with 10 μM rotenone to induce cell toxicity. We assessed cell death by Western blotting using specific antibodies, such as phospho-ERK1/2, phospho-JNK, and cleaved capase-3 and performed an MTT assay for evaluation of cell death and mitochondria staining. Pretreatment with 2.5 μg/mL BV had a neuroprotective effect against 10 μM rotenone-induced cell death in NSC34 motor neuron cells. Pre-treatment with BV significantly enhanced cell viability and ameliorated mitochondrial impairment in rotenone-treated cellular model. Moreover, BV treatment inhibited the activation of JNK signaling and cleaved caspase-3 related to cell death and increased ERK phosphorylation involved in cell survival in rotenone-treated NSC34 motor neuron cells. Taken together, we suggest that BV treatment can be useful for protection of neurons against oxidative stress or neurotoxin-induced cell death. View Full-Text
Keywords: bee venom (BV); NSC34 motor neuron cell; rotenone; phospho-JNK; cleaved caspase-3 bee venom (BV); NSC34 motor neuron cell; rotenone; phospho-JNK; cleaved caspase-3
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Jung, S.Y.; Lee, K.-W.; Choi, S.-M.; Yang, E.J. Bee Venom Protects against Rotenone-Induced Cell Death in NSC34 Motor Neuron Cells. Toxins 2015, 7, 3715-3726.

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