2009Unpublished venueRequires access

Interleukin-6 prevents NMDA-induced apoptosis of the cultured cerebellar granule neurons

Huang Yan

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Abstract

Objective: We explored that IL-6 protected neurons against NMDA-induced apoptosis at the gene levels of anti- apoptotic Bcl-2, pro-apoptotic Bax and apoptotic enzyme cysteinyl asparate-specific proteinase-3 (caspase-3). Methods: The cerebellar granule neurons from postnatal 8-day infant rats were chronically exposed to IL-6 (40 ng/ml), NMDA (100 μmol/L) was then added to the cultures and stimulated the neurons for 30 min to induce the neuronal apoptosis. Real- time PCR was employed to detect the expression of genes related to neuronal apoptosis, including Bcl-2, Bax and caspase-3. Results: NMDA stimulation of the cultured cerebellar granule neurons without IL-6 pretreatment led to a notable reduction of Bcl-2 mRNA expression, as well as a remarkable enhancement of Bax and caspase-3 mRNA expression. The NMDA stimu- lation of the neurons that had been pretreated with IL-6 caused a remarkable increase in Bcl-2 mRNA expression, as well as a marked decrease in Bax and caspase-3 mRNA expression in comparison with those of neurons lacking IL-6 pretreatment. Conclusions: NMDA can induce neuronal apoptosis. Chronic IL-6 exposure can protect neurons against NMDA-induced neu- ronal apoptosis.

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Objective: We explored that IL-6 protected neurons against NMDA-induced apoptosis at the gene levels of anti- apoptotic Bcl-2, pro-apoptotic Bax and apoptotic enzyme cysteinyl asparate-specific proteinase-3 (caspase-3). Methods: The cerebellar granule neurons from postnatal 8-day infant rats were chronically exposed to IL-6 (40 ng/ml), NMDA (100 μmol/L) was then added to the cultures and stimulated the neurons for 30 min to induce the neuronal apoptosis. Real- time PCR was employed to detect the expression of genes related to neuronal apoptosis, including Bcl-2, Bax and caspase-3. Results: NMDA stimulation of the cultured cerebellar granule neurons without IL-6 pretreatment led to a notable reduction of Bcl-2 mRNA expression, as well as a remarkable enhancement of Bax and caspase-3 mRNA expression. The NMDA stimu- lation of the neurons that had been pretreated with IL-6 caused a remarkable increase in Bcl-2 mRNA expression, as well as a marked decrease in Bax and caspase-3 mRNA expression in comparison with those of neurons lacking IL-6 pretreatment. Conclusions: NMDA can induce neuronal apoptosis. Chronic IL-6 exposure can protect neurons against NMDA-induced neu- ronal apoptosis.

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Available abstract

Objective: We explored that IL-6 protected neurons against NMDA-induced apoptosis at the gene levels of anti- apoptotic Bcl-2, pro-apoptotic Bax and apoptotic enzyme cysteinyl asparate-specific proteinase-3 (caspase-3). Methods: The cerebellar granule neurons from postnatal 8-day infant rats were chronically exposed to IL-6 (40 ng/ml), NMDA (100 μmol/L) was then added to the cultures and stimulated the neurons for 30 min to induce the neuronal apoptosis. Real- time PCR was employed to detect the expression of genes related to neuronal apoptosis, including Bcl-2, Bax and caspase-3. Results: NMDA stimulation of the cultured cerebellar granule neurons without IL-6 pretreatment led to a notable reduction of Bcl-2 mRNA expression, as well as a remarkable enhancement of Bax and caspase-3 mRNA expression. The NMDA stimu- lation of the neurons that had been pretreated with IL-6 caused a remarkable increase in Bcl-2 mRNA expression, as well as a marked decrease in Bax and caspase-3 mRNA expression in comparison with those of neurons lacking IL-6 pretreatment. Conclusions: NMDA can induce neuronal apoptosis. Chronic IL-6 exposure can protect neurons against NMDA-induced neu- ronal apoptosis.

Key concepts: Apoptosis, NMDA receptor, Granule (geology), Messenger RNA, Caspase, Cerebellum, Cell biology, Caspase 3

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