ArticleToxins2015
Bee Venom Protects against Rotenone-Induced Cell Death in NSC34 Motor Neuron Cells.
Article in Toxins, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- Melittin inhibits MPPThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- Heterologous expressing melittin in a probiotic yeast to evaluate its function for promoting NSC-34 regeneration.Applied microbiology and biotechnology · 2024Article
- The gill epithelial cell lines RTgill-W1, from Rainbow trout and ASG-10, from Atlantic salmon, exert different toxicity profiles towards rotenone.Cytotechnology · 2023Article
- Protective Effects of Bee Venom-Derived Phospholipase ABiomedicines · 2021Article
- Vulnerability of subcellular structures to pathogenesis induced by rotenone in SH-SY5Y cells.Physiological research · 2021Article
- Bee Venom in Wound Healing.Molecules (Basel, Switzerland) · 2020Review
- Bee venom attenuates neurodegeneration and motor impairment and modulates the response to L-dopa or rasagiline in a mice model of Parkinson's disease.Iranian journal of basic medical sciences · 2020Article
- Bee Venom: An Updating Review of Its Bioactive Molecules and Its Health Applications.Nutrients · 2020Review
- Article
- Protective Effects of Bee Venom against Endotoxemia-Related Acute Kidney Injury in Mice.Biology · 2020Article
- Bee Venom: Overview of Main Compounds and Bioactivities for Therapeutic Interests.Molecules (Basel, Switzerland) · 2019Review
- Midazolam prevents motor neuronal death from oxidative stress attack mediated by JNK-ERK pathway.Human cell · 2018Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
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