Journal
TOXICOLOGY LETTERS
Volume 238, Issue 3, Pages 70-82Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.toxlet.2015.08.011
Keywords
Pyrroloquinoline quinone (PQQ); Rotenone; Neuroprotection; Reactive oxygen species (ROS); Parkinson's disease (PD); Dopamine
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Funding
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
- National Natural Science Foundation of China [81171180, 81201017]
- Natural Science Funding from the Education Department of Jiangsu Province, China [12KJB310011]
- practice innovation training program projects for the Jiangsu College students [201410304065Y]
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Pyrroloquinoline quinone (PQQ), a redox cofactor in the mitochondrial respiratory chain, has proven to protect neurons against glutamate-induced damage both in vitro and in vivo. This study was aimed to investigate the possible neuroprotective effects of PQQ in rotenone-induced Parkinson's disease (PD) model. Pre-treatment with PQQ prevented cultured SH-SY5Y cells from rotenone-induced apoptosis, accompanied by modulation of apoptosis-related proteins (Bcl-2, Bax and Smac), restoration of the mitochondrial membrane potential, inhibition of intracellular reactive oxygen species (ROS) production, suppression of tyrosine residues nitration, and dopamine redistribution. PQQ also exerted protective effects in an in vivo PD model, which was created by rotenone injection into the medial forebrain bundle of rats. Co-injection with PQQ and rotenone improved the apomorphine-evoked rotation, decreased neuronal loss, increased the ROS-scavenging ability, regulated intracellular expressions of mitochondrial complex subunits (Ndufs1-4), tyrosine hydroxylase, and vesicular monoamine transporter 2. Taken together, our results collectively suggest that PQQ confers neuroprotection in rotenone-induced PD model probably through complex and multifaceted mechanisms, at least involving oxidative stress, mitochondrial integrity, and dopamine functions. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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