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

Jung SY, Lee KW, Choi SM, Yang EJ - Toxins (Basel) (2015)

Bottom Line: In this study, we tested the effects of BV on neuronal cell death by examining rotenone-induced mitochondrial dysfunction.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.

View Article: PubMed Central - PubMed

Affiliation: Department 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.

No MeSH data available.


Related in: MedlinePlus

BV pretreatment prevents rotenone-induced cytotoxicity in NSC34 neuronal cells. (A) NSC34 cells were treated with 10 µM rotenone for 0, 3, 6, 12, and 24 h and cell viability was determined using MTT assay. 10 µM rotenone treatment induced time-dependent cytotoxicity in NSC34 cells; (B) NSC34 cells were treated with 2.5 µg/mL BV prior to stimulation with 10 µM rotenone for 24 h. BV pretreatment prevented 10 µM rotenone-induced cytotoxicity in NSC34 cells. The values shown are the means ±S.E.M. of data obtained from three independent experiments. *p < 0.05, ***p < 0.001.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4591667&req=5

toxins-07-03715-f001: BV pretreatment prevents rotenone-induced cytotoxicity in NSC34 neuronal cells. (A) NSC34 cells were treated with 10 µM rotenone for 0, 3, 6, 12, and 24 h and cell viability was determined using MTT assay. 10 µM rotenone treatment induced time-dependent cytotoxicity in NSC34 cells; (B) NSC34 cells were treated with 2.5 µg/mL BV prior to stimulation with 10 µM rotenone for 24 h. BV pretreatment prevented 10 µM rotenone-induced cytotoxicity in NSC34 cells. The values shown are the means ±S.E.M. of data obtained from three independent experiments. *p < 0.05, ***p < 0.001.

Mentions: To examine the cytotoxicity of NSC34 cells after rotenone treatment, we incubated NSC34 motor neuron cells with 10 μM rotenone for various time periods (0, 3, 6, 12, and 24 h). Our results showed that rotenone decreased cell survival in a time-dependent manner (Figure 1A). Compared to untreated NSC34 cells, 10 μM rotenone treatment for 24 h resulted in a 37% decrease in cell viability. To investigate whether BV attenuates rotenone-induced cytotoxicity, we performed a cell viability test on the cells treated with 10 μM rotenone for 24 h with or without 2.5 µg/mL BV pretreatment. BV pretreatment prevented cell death induced by 10 μM rotenone, with about 29% protection for a dose of 2.5 µg/mL BV compared to rotenone-treated cells (Figure 1B). These results indicate that BV pretreatment had a protective effect against rotenone-induced cytotoxicity.


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

Jung SY, Lee KW, Choi SM, Yang EJ - Toxins (Basel) (2015)

BV pretreatment prevents rotenone-induced cytotoxicity in NSC34 neuronal cells. (A) NSC34 cells were treated with 10 µM rotenone for 0, 3, 6, 12, and 24 h and cell viability was determined using MTT assay. 10 µM rotenone treatment induced time-dependent cytotoxicity in NSC34 cells; (B) NSC34 cells were treated with 2.5 µg/mL BV prior to stimulation with 10 µM rotenone for 24 h. BV pretreatment prevented 10 µM rotenone-induced cytotoxicity in NSC34 cells. The values shown are the means ±S.E.M. of data obtained from three independent experiments. *p < 0.05, ***p < 0.001.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4591667&req=5

toxins-07-03715-f001: BV pretreatment prevents rotenone-induced cytotoxicity in NSC34 neuronal cells. (A) NSC34 cells were treated with 10 µM rotenone for 0, 3, 6, 12, and 24 h and cell viability was determined using MTT assay. 10 µM rotenone treatment induced time-dependent cytotoxicity in NSC34 cells; (B) NSC34 cells were treated with 2.5 µg/mL BV prior to stimulation with 10 µM rotenone for 24 h. BV pretreatment prevented 10 µM rotenone-induced cytotoxicity in NSC34 cells. The values shown are the means ±S.E.M. of data obtained from three independent experiments. *p < 0.05, ***p < 0.001.
Mentions: To examine the cytotoxicity of NSC34 cells after rotenone treatment, we incubated NSC34 motor neuron cells with 10 μM rotenone for various time periods (0, 3, 6, 12, and 24 h). Our results showed that rotenone decreased cell survival in a time-dependent manner (Figure 1A). Compared to untreated NSC34 cells, 10 μM rotenone treatment for 24 h resulted in a 37% decrease in cell viability. To investigate whether BV attenuates rotenone-induced cytotoxicity, we performed a cell viability test on the cells treated with 10 μM rotenone for 24 h with or without 2.5 µg/mL BV pretreatment. BV pretreatment prevented cell death induced by 10 μM rotenone, with about 29% protection for a dose of 2.5 µg/mL BV compared to rotenone-treated cells (Figure 1B). These results indicate that BV pretreatment had a protective effect against rotenone-induced cytotoxicity.

Bottom Line: In this study, we tested the effects of BV on neuronal cell death by examining rotenone-induced mitochondrial dysfunction.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.

View Article: PubMed Central - PubMed

Affiliation: Department 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.

No MeSH data available.


Related in: MedlinePlus