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KMID : 0356620140290030371
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Journal of Korean Society of Endocrinology
2014 Volume.29 No. 3 p.371 ~ p.378
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Ghrelin Inhibits Oligodendrocyte Cell Death by Attenuating Microglial Activation
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Lee Jee-Youn
Yune Tae-Young
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Abstract
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Background: Recently, we reported the antiapoptotic effect of ghrelin in spinal cord injury-induced apoptotic cell death of oligodendrocytes. However, how ghrelin inhibits oligodendrocytes apoptosis, is still unknown. Therefore, in the present study, we examined whether ghrelin inhibits microglia activation and thereby inhibits oligodendrocyte apoptosis.
Methods: Using total cell extracts prepared from BV-2 cells activated by lipopolysaccharide (LPS) with or without ghrelin, the levels of p-p38 phosphor-p38 mitogen-activated protein kinase (p-p38MAPK), phospho-c-Jun N-terminal kinase (pJNK), p-c-Jun, and pro-nerve growth factor (proNGF) were examined by Western blot analysis. Reactive oxygen species (ROS) production was investigated by using dichlorodihydrofluorescein diacetate. To examine the effect of ghrelin on oligodendrocyte cell death, oligodendrocytes were cocultured in transwell chambers of 24-well plates with LPS-stimulated BV-2 cells. After 48 hours incubation, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and terminal deoxynucleotidyl transferase 2’-deoxyuridine, 5’-triphosphate nick end labeling staining were assessed.
Results: Ghrelin treatment significantly decreased levels of p-p38MAPK, p-JNK, p-c-Jun, and proNGF in LPS-stimulated BV-2 cells. ROS production increased in LPS-stimulated BV-2 cells was also significantly inhibited by ghrelin treatment. In addition, ghrelin significantly inhibited oligodendrocyte cell death when cocultured with LPS-stimulated BV-2 cells.
Conclusion: Ghrelin, p38MAPK, c-Jun N-terminal kinase, Pro-nerve growth factor, Reactive oxygen species, Oligodendroglia, BV-2 microglia cell.
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KEYWORD
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Ghrelin, p38MAPK, c-Jun N-terminal kinase, Pro-nerve growth factor, Reactive oxygen species, Oligodendroglia, BV-2 microglia cell
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