Premium
S‐52, a novel nootropic compound, protects against β‐amyloid induced neuronal injury by attenuating mitochondrial dysfunction
Author(s) -
Gao Xin,
Zheng Chun Yan,
Qin Guo Wei,
Tang Xi Can,
Zhang Hai Yan
Publication year - 2012
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.23086
Subject(s) - neuroprotection , nootropic , oxidative stress , mitochondrion , reactive oxygen species , pharmacology , chemistry , biochemistry , microbiology and biotechnology , biology
Accumulating evidence suggests that β‐amyloid (Aβ)‐induced oxidative DNA damage and mitochondrial dysfunction may initiate and contribute to the progression of Alzheimer's disease (AD). This study evaluated the neuroprotective effects of S‐52, a novel nootropic compound, on Aβ‐induced mitochondrial failure. In an established paradigm of moderate cellular injury induced by Aβ, S‐52 was observed to attenuate the toxicity of Aβ to energy metabolism, mitochondrial membrane structure, and key enzymes in the electron transport chain and tricarboxylic acid cycle. In addition, S‐52 also effectively inhibited reactive oxygen species accumulation dose dependently not only in Aβ‐harmed cells but also in unharmed, normal cells. The role of S‐52 as a scavenger of free radicals is involved in the antioxidative effect of this compound. The beneficial effects on mitochondria and oxidative stress extend the neuroprotective effects of S‐52. The present study provides crucial information for better understanding the beneficial profiles of this compound and discovering novel potential drug candidates for AD therapy. © 2012 Wiley Periodicals, Inc.