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Bee Venom Protects against Rotenone-Induced Cell Death in NSC34 Motor Neuron Cells
So Young Jung1, Kang-Woo Lee2, Sun-Mi Choi3
1Department of Medical Research, Korea Institute of Oriental Medicine, 483 Expo-ro, Yuseong-gu, Daejeon 305-811, Korea. syzzim84@gmail.com.
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.
Insights
Bee venom (BV) protects motor neurons from rotenone-induced cell death by preserving mitochondrial function. BV treatment inhibits apoptosis pathways and enhances cell survival signaling, suggesting its neuroprotective potential.
Area of Science:
- Neuroscience
- Toxicology
- Biochemistry
Background:
- Rotenone inhibits mitochondrial complex I, increasing reactive oxygen species and apoptosis via caspase-3.
- Bee venom (BV) contains bioactive compounds and has traditional medicinal uses.
- Investigating BV's effects on rotenone-induced neuronal damage is crucial.
Purpose of the Study:
- To evaluate the neuroprotective effects of bee venom against rotenone-induced mitochondrial dysfunction and cell death.
- To determine the impact of BV pretreatment on neuronal cell viability and apoptosis markers.
- To elucidate the signaling pathways modulated by BV in a rotenone-induced cellular model.
Main Methods:
- NSC34 motor neuron cells were pretreated with bee venom (2.5 μg/mL) followed by rotenone (10 μM) exposure.
- Cell death was assessed using MTT assays and Western blotting for apoptosis markers (caspase-3) and signaling proteins (ERK, JNK).
- Mitochondrial function was evaluated through specific staining techniques.
Main Results:
- Bee venom pretreatment significantly enhanced cell viability in rotenone-treated NSC34 motor neurons.
- BV ameliorated rotenone-induced mitochondrial impairment and inhibited the activation of JNK signaling and cleaved caspase-3.
- BV treatment increased ERK phosphorylation, a marker associated with cell survival.
Conclusions:
- Bee venom exhibits significant neuroprotective effects against rotenone-induced toxicity in motor neurons.
- BV mitigates neuronal cell death by preserving mitochondrial function and modulating key apoptotic and survival signaling pathways.
- Bee venom holds promise as a therapeutic agent for neuroprotection against oxidative stress and neurotoxins.
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