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PACAP38 protects against sodium nitroprusside‐induced apoptosis in rat cortical neurons
Author(s) -
Sanchez Alma,
Grammas Paula
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a20-c
Subject(s) - neuroprotection , neurotoxicity , sodium nitroprusside , neurodegeneration , vasoactive intestinal peptide , endocrinology , neurotrophin , apoptosis , medicine , neurotrophic factors , neuropeptide , programmed cell death , nitric oxide , chemistry , pharmacology , biochemistry , toxicity , receptor , disease
Pituitary adenylate cyclase‐activating polypeptide (PACAP38) is a multifunctional neuropeptide and a member of the vasoactive intestinal peptide family. It functions as a hypothalamic hormone, neurotransmitter, neuromodulator, and neurotrophic factor. PACAP38 has been shown to be neuroprotective in some animal models of neurodegeneration. The objective of this study was to determine whether PACAP38 was protective against the neurotoxicity induced by sodium nitroprusside (SNP), an nitric oxide (NO) donor. Treatment of primary cortical neuronal cultures with 1 mM SNP for 4 h caused neuronal cell death that was significantly reduced by 100 nM PACAP38. We also examined the ability of PACAP38 to alter SNP induced expression of cell death associated proteins. Our results indicated that PACAP38 downregulated SNP‐induced cell cycle protein (cyclin E) and pro‐apoptotic protein (Bad) expression. The neuroprotective effects of PACAP38 against SNP‐induced apoptosis support the possibility that PACAP38 could reduce neurodegeneration in the brain in diseases such as Alzheimer's disease where NO‐mediated neurotoxicity has been implicated.