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Journal of Biotechnology and Phytochemistry
Volume 1 Issue 3 Chemistry World 2017
Notes:
Page 41
November 13-15, 2017 Athens, Greece
7th World Congress on
Chemistry
N-acetyl serotonin protects neuronal cell death induced
by oxidative stress via elevation of TrkB/CREB/BDNF
and Akt/Nrf2 pathways
Mee Ree Kim
Chungnam National University, South Korea
Recently, N-acyl serotonin, present in the intestine, has
been reported to exert neuroprotective action against
oxidative stress by inducing antioxidant enzymes. However,
the mechanism for neuroprotective action of N-acetyl
serotonin(NAS) as a precursor of melatonin is not clarified.
In this study we focused on the suppressive effect of N-acetyl
serotonin on glutamate-induced apoptosis in HT-22 cells,
and then examined the molecular mechanism for its anti-
apoptotic action. For this purpose, we performed flow
cytometry, immunoblotting analyses and antibody-mediated
neutralization.WhenHT-22 cellswere preincubatedwithNAS
prior to glutamate treatment, NAS dose-dependently reduced
apoptotic bodies and recovered mitochondrial potential
in glutamate-treated HT-22 cells. NAS dose-dependently
inhibited oxidative stress-induced cell death in HT-22 cells.
Moreover, NAS suppressed glutamate-induced apoptosis by
suppressing expression of pro-apoptotic factors such as AIF,
Bax, calpain, cytochrome c and cleaved caspase-3, whereas
it enhanced expression of Bcl-2, an anti-apoptotic factor. In
addition, NAS improved phosphorylation of tropomyosin-
related kinase receptor (TrkB) and cAMP response element-
binding protein (CREB) as well as expression of brain-derived
neurotrophic factor (BDNF), whereas the inclusion of each
inhibitor of JNK, p38 or Akt neutralized the neuroprotective
effect of NAS, but not that of ERK. Meanwhile, NAS dose-
dependently reduced the level of reactive oxygen species,
and enhanced the level of glutathione in glutamate-treated
HT-22 cells. Moreover, NAS not only increased expression of
heme oxygenase-1, NAD(P)H quinine oxidoreductase-1 and
glutamate-cysteine ligase catalytic subunit, but also enhanced
nuclear translocation of NF-E2-related factor-2. Separately,
NAS at 30 mg/kg suppressed scopolamine-induced memory
impairment and cell death in CA1 and CA3 regions in
mice. In conclusion, NAS shows actions of antioxidant and
anti-apoptosis by activating TrkB/CREB/BDNF pathway
and expression of antioxidant enzymes in oxidative stress-
induced neurotoxicity. Therefore, such effects of NAS may
provide the information for the application of NAS against
neurodegenerative diseases.
Biography
Mee Ree Kim has completed her PhD from Seoul National University and is a
Visiting Professor at Wisconsin-Madison University, Department of Toxicology.
She is the former President of Korean Food Related Academic Association. She
has published more than 120 papers in reputed journals and has been serving
as an Editorial Board Member of repute such as Journal of Medicinal Food.
Mee Ree Kim, J Biotech and Phyto 2017