期刊
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
卷 31, 期 1, 页码 233-241出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.etap.2010.11.002
关键词
Baicalein; Reactive oxygen species; Mitochondrial dysfunction; Oxidative stress; Manganese superoxide dismutase
资金
- Ministry of Science & Technology (MOST) of Korea
This study investigated the cytoprotective effect of baicalein (5,6,7-trihydroxyflavone) against oxidative stress-induced mitochondrial dysfunction. Electron spin resonance (ESR) spectrometry revealed that baicalein showed significant scavenging effects on superoxide radicals and hydroxyl radicals. When H2O2 treatment induces an increase in mitochondrial reactive oxygen species (ROS), baicalein treatment decreased high level of ROS. Baicalein significantly reduced alteration of Bcl-2 family proteins, the release of cytochrome c from mitochondria into the cytosol via inhibition of mitogen-activated protein kinase kinase-4 (MKK4/SEK1) and c-Jun NH2-terminal kinase (JNK) cascades induced by H2O2 treatment. Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme in mitochondria against oxidative stress. Baicalein restored both MnSOD protein expression and activity, which were abolished by H2O2 treatment. The transcription factor NF-E2-related factor 2 (Nrf2) is a critical regulator of MnSOD, achieved by binding to the antioxidant response element (ARE). Baicalein restored nuclear Nrf2 protein expression and its ARE binding activity, which were abolished by H2O2 treatment. These studies demonstrate that baicalein attenuates mitochondrial oxidative stress by activating Nrf2-mediated MnSOD induction. (C) 2010 Elsevier B.V. All rights reserved.
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