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.
Highlights
Rotenone is a naturally-occurring plant compound and a specific inhibitor of complex I of the mitochondrial respiration chain
The present study demonstrates that Bee venom (BV) reduces rotenone-induced cell death in NSC34 cells by blocking the Jun N-terminal kinase (JNK) and ERK1/2 signaling pathways
The MAPK family, including ERK1/2, stress-activated protein kinase/c-jun NH4-terminal kinase (SAPK/JNK), and p38 MAPKs [22,23], play central roles in the signaling pathways involved in cell proliferation, survival, and apoptosis
Summary
Rotenone is a naturally-occurring plant compound and a specific inhibitor of complex I of the mitochondrial respiration chain. Microglial activation, oxidative damage, dopaminergic degeneration, and L-dopa-responsive motor deficit. Rotenone was thought to elevate mitochondrial reactive oxygen species production [1], decreasing cellular ATP levels [2] and mitochondrial membrane potential [3]. Other reports have indicated that rotenone induces apoptosis via an increase in mitochondria reactive oxygen species production and neurotoxicity associated with increased levels of caspase family gene expression [4] in PC12 cells. Bee venom (BV) is known to be a very complex mixture of active peptides including melittin, phospholipase A2, apamin, adolapin, and mast cell-degranulating peptide [5].
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