Olfactory ensheathing cell-conditioned medium reverts 3 Ab25–35-induced oxidative damage in SH-SY5Y cells 4 by modulating the mitochondria-mediated apoptotic pathway.
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2016
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Cellular and Molecular Neurobiology
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Abstract
Olfactory ensheathing cells (OECs) are a type of
10 glia from the mammalian olfactory system, with neuro-
11 protective and regenerative properties. b-Amyloid peptides
12 are a major component of the senile plaques characteristic
13 of the Alzheimer brain. The amyloid beta (Ab) precursor
14 protein is cleaved to amyloid peptides, and Ab25–35 is
15 regarded to be the functional domain of Ab, responsible for
16 its neurotoxic properties. It has been reported that Ab25–35
17 triggers reactive oxygen species (ROS)-mediated oxidative
18 damage, altering the structure and function of mitochon-
19 dria, leading to the activation of the mitochondrial intrinsic
20 apoptotic pathway. Our goal is to investigate the effects of
21 OECs on the toxicity of aggregated Ab25–35, in human
22 neuroblastoma SH-SY5Y cells. For such purpose, SH-
23 SY5Y cells were incubated with Ab25–35 and OEC-conditioned medium (OECCM). OECCM promoted the 24
cell viability and reduced the apoptosis, and decreased the 25
intracellular ROS and the lipid peroxidation. In the pres- 26
ence of OECCM, mRNA and protein levels of antioxidant 27
enzymes (SOD1 and SOD2) were upregulated. Concomi- 28
tantly, OECCM decreased mRNA and the protein expres- 29
sion levels of cytochrome c, caspase-9, caspase-3, and Bax 30
in SH-SY5Y cells, and increased mRNA and the protein 31
expression level of Bcl-2. However, OECCM did not alter 32
intracellular Ca 33 2? concentration in SH-SY5Y cells. Taken
together, our data suggest that OECCM ameliorates 34
Ab25–35-induced oxidative damage in neuroblastoma SH- 35
SY5Y cells by inhibiting the mitochondrial intrinsic path- 36
way. These data provide new insights into the functional 37
actions of OECCM on oxidative stress-induced cell 38
damage.
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Keywords
Alzheimer’s disease, Olfactory ensheathing cells, Oxidative damage, Mitochondria, Apoptosis