Abstract：
: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 H(2)O(2) 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 NH(2)-terminal kinase (JNK) cascades induced by H(2)O(2) 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 H(2)O(2) 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 H(2)O(2) treatment. These studies demonstrate that baicalein attenuates mitochondrial oxidative stress by activating Nrf2-mediated MnSOD induction.
journal_name
Environ Toxicol Pharmacoljournal_title
Environmental toxicology and pharmacologyauthors
Lee IK,Kang KA,Zhang R,Kim BJ,Kang SS,Hyun JWdoi
10.1016/j.etap.2010.11.002subject
Has Abstractpub_date
2011-01-01 00:00:00pages
233-41issue
1eissn
1382-6689issn
1872-7077pii
S1382-6689(10)00184-5journal_volume
31pub_type
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