Coenzyme Q10 protects SHSY5Y neuronal cells from beta amyloid
toxicity and oxygen-glucose deprivation by inhibiting the opening of the
mitochondrial permeability transition pore
Issue title: The Fourth Conference of the International
CoQ10 Association
Affiliations: The Jockey Club MRI Centre, The University of Hong
Kong, Hong Kong, China | Department of Neurology, The First Affiliated
Hospital, Harbin Medical University, China | Institute of Molecular Medicine, Peking University,
China
Note: [] Address for correspondence: Geng Li, The Jockey Club MRI Centre,
The University of Hong Kong, Room 204, Chow Yei Ching Bldg., Pokfulam Road,
Hong Kong. Tel.: +852 2293 0305; Fax: +852 2540 6215; E-mail: ligeng@eee.hku.hk
Abstract: Coenzyme Q10 (CoQ10) is an essential biological cofactor which
increases brain mitochondrial concentration and exerts neuroprotective effects.
In the present study, we exposed SHSY5Y neuroblastoma cells to neurotoxic beta
amyloid peptides (Aβ) and oxygen glucose deprivation (OGD) to investigate
the neuroprotective effect of 10μM CoQ10 by measuring (i) cell viability by
the MTT assay, (ii) opening of the mitochondrial permeability transition pore
via the fluorescence intensity of calcein-AM, and (iii) superoxide anion
concentration by hydroethidine. Cell viability (mean ±
S.E.M.) was 55.5 ± 0.8% in the group exposed to Aβ + OGD, a
value lower than that in the Aβ or OGD group alone (P<0.01). CoQ10 had
no neuroprotective effect on cell death induced by either Aβ or OGD, but
increased cell survival in the Aβ + OGD group to 57.3 ± 1.7%,
which was higher than in the group treated with vehicle (P<0.05). The
neuroprotective effect of CoQ10 was blocked by administration of 20μM
atractyloside. Pore opening and superoxide anion concentration were increased
in the Aβ + OGD group relative to sham control (P<0.01), and were
attenuated to the sham level (P>0.05) when CoQ10 was administered. Our
results demonstrate that CoQ10 protects neuronal cells against Aβ
neurotoxicity together with OGD by inhibiting the opening of the pore and
reducing the concentration of superoxide anion.
