Notes:
Volume 6, Issue 4 (Suppl)
Clin Pharmacol Biopharm, an open access journal
ISSN: 2167-065X
Page 23
Euro Biopharma & Ethnopharmacology 2017
November 09-11, 2017
&
6
th
International Conference and Exhibition on
November 09-11, 2017 Vienna, Austria
4
th
EUROPEAN BIOPHARMA CONGRESS
PHARMACOLOGY AND ETHNOPHARMACOLOGY
Joint Event
Harnessing phytochemicals to protect neuronal and glial cells from oxidative stress
Anat Elmann
1
, Alona Telerman
1
Sharon Mordechay
1
, Hilla Erlank
1
, Rivka Ofir
2
and
Yoel Kashman
3
1
Agricultural Research Organization, Austria
2
Dead Sea and Arava Science Center, Austria
3
Tel Aviv University, Austria
O
xidative stress and amyloidbeta toxicity are involved in the pathogenesis of Alzheimer's
diseases.Wehave previously demonstrated
that an extract prepared of the plant
Achillea fragrantissima
(
Af)
protected cultured brain astrocytes from oxidative stress-
induced cell death and down regulated microglial activation. Using activity guided fractionation, we have purified from Af an active
flavonoid named 3,5,4-trihydroxy-6,7,3-trimethoxyflavone (TTF). TTF protected cultured astrocytes from H
2
O
2
–induced cell death
via interference with cell signaling (inhibition of SAPK/JNK, ERK 1/2, and MEK1 phosphorylation) and by reducing the levels of
oxidative stress-induced intracellular reactive oxygen species (ROS). The mechanism of the protective effect of TTF against H
2
O
2
-
cytotoxicity could not be attributed to a direct H
2
O
2
scavenging but rather to the scavenging of free radicals as was shown in cell free
systems. In addition, TTF protected cultured neuronal cells from amyloid beta cytotoxicity via interference with cell signaling events
and by reducing the amyloid beta - induced levels of intracellular ROS. Moreover, TTF exhibited anti-inflammatory activities and
inhibited the LPS-elicited secretion of the proinflammatory cytokines Interleukin 6 (IL-6) and IL-1beta from microglial cells. Our
results suggest that TTF might be a therapeutic candidate for the treatment of Alzheimer’s disease as well as other neurodegenerative
diseases where oxidative stress, neuroinflammation and amyloid beta toxicity are part of the pathophysiology.
aelmann@volcani.agri.gov.ilAnat Elmann et al., Clin Pharmacol Biopharm 2017, 6:4(Suppl)
DOI: 10.4172/2167-065X-C1-025