Protective effects of lipopolysaccharide preconditioning against nitric oxide neurotoxicity
| ISSN: | 1097-4547 0360-4012 |
|---|---|
| Přístupová URL adresa: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9009e5dcbabc2c395e523940a0d0c23f https://doi.org/10.1002/jnr.21594 |
| Rights: | CLOSED |
| Přírůstkové číslo: | edsair.doi.dedup.....9009e5dcbabc2c395e523940a0d0c23f |
| Autor: | Fu-Zen Shaw, Hui I. Yang, Shang-Der Chen, Chia Yen Huang, Ding I. Yang |
| Rok vydání: | 2008 |
| Předmět: |
Lipopolysaccharides
Nitric Oxide Synthase Type III Blotting Western Pharmacology Nitric Oxide Neuroprotection Nitric oxide Rats Sprague-Dawley Cellular and Molecular Neuroscience chemistry.chemical_compound Enos medicine Animals Nitric Oxide Donors Ischemic Preconditioning Protein kinase A Cyclic GMP Cells Cultured Neurons Microscopy Confocal biology Neurotoxicity Brain biology.organism_classification medicine.disease Immunohistochemistry NONOate Rats Microscopy Fluorescence Proto-Oncogene Proteins c-bcl-2 chemistry Biochemistry Nerve Degeneration Sodium nitroprusside cGMP-dependent protein kinase Signal Transduction medicine.drug |
| Zdroj: | Journal of Neuroscience Research. 86:1277-1289 |
| ISSN: | 1097-4547 0360-4012 |
| Popis: | We have characterized lipopolysaccharide (LPS) preconditioning-induced neuroprotective mechanisms against nitric oxide (NO) toxicity. Pretreatment of rat cortical cultures with LPS attenuated neurotoxicity of NO donors, including sodium nitroprusside (SNP) and diethylamine NONOate (NONOate). A transiently increased expression of endothelial nitric oxide synthase (eNOS) accompanied by an increase in NO production was observed during LPS preconditioning. Application of NOS inhibitors including L-N(5)-(1-iminoethyl)-ornithine (L-NIO) and L-nitroarginine methylester (L-NAME) abolished LPS-dependent protection against SNP toxicity. The LPS effect was also blocked by KT5823, an inhibitor of cGMP-dependent protein kinase (PKG). Consistently, application of 8-bromo-cyclic GMP (8-Br-cGMP), a slowly degradable cGMP analogue capable of PKG activation, was neuroprotective. LPS preconditioning resulted in a heightened neuronal expression of Bcl-2 protein that was abolished by L-NAME and KT5823, the respective inhibitors of NOS and PKG. Together, our results reveal the signaling cascade of "LPS --> eNOS --> NO --> cGMP/PKG --> Bcl-2" that might have contributed to the LPS protective effects in cortical neurons. |
| Databáze: | OpenAIRE |
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