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Cinnamon decreases excitation toxicity in primary neuronal cultures from chick embryos
Author(s) -
Gomada Yuki,
Jamison Brandon Y,
Maitin Vatsala,
Vattem Dhiraj A.
Publication year - 2012
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.26.1_supplement.1025.11
Subject(s) - toxicity , neuroprotection , neurotoxicity , glutamate receptor , programmed cell death , viability assay , pharmacology , embryo , chemistry , biology , cell , microbiology and biotechnology , medicine , apoptosis , biochemistry , receptor
Excitation neurotoxicity induced dysregulation of stress response signaling has been implicated in neurodegenerative pathologies such as Alzheimer's disease and Parkinson's disease. Cinnamon was previously reported to beneficially modulate stress response signaling in C. elegans and may have therapeutic potential. The objective here was to evaluate the dose dependent neuroprotective effect of cinnamon on L‐glutamate and NDMA induced excitation toxicity in cultured primary neurons from chick embryos. Results suggest that cinnamon treatment decreased neuronal cell death in L‐glutamate and NDMA induced excitation toxicity by 20% and 15% respectively. Evaluation with fractionated cinnamon extract characterized by HPLC/DAD/ELSD/MS suggests that protection against L‐glutamate toxicity was primarily due to the polar neutral fraction which increased neuronal cell survival by 23%. Neuroprotective effects in NDMA treated primary cultures were predominantly due to polar basic fraction which decreased cell death by 25% compared to control. Grant Funding Source : VRDÜR Foundation