Research Papers: Gerotarget (Focus on Aging):
Baicalein is an available anti-atherosclerotic compound through modulation of nitric oxide-related mechanism under oxLDL exposure
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Shih-Hung Chan1, Ching-Hsia Hung2,3, Jhih-Yuan Shih4, Pei-Ming Chu5, Yung-Hsin Cheng6, Yi-Ju Tsai3, Huei-Chen Lin2,7 and Kun-Ling Tsai3
1 Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan
2 Institute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan
3 Department of Physical Therapy, College of Medicine, National Cheng Kung University, Tainan, Taiwan
4 Department of Internal Medicine, Chi-Mei Hospital, Tainan, Taiwan
5 Department of Anatomy, School of Medicine, China Medical University, Taichung, Taiwan
6 Department of Education and Research, Taipei City Hospital, Taipei, Taiwan
7 Department of Physical Therapy, Shu-Zen Junior College of Medicine and Management, Kaohsiung, Taiwan
Kun-Ling Tsai, email:
Keywords: oxidized low-density lipoprotein, endothelial cells, baicalein, nitric oxide, reactive oxygen species, Gerotarget
Received: April 25, 2016 Accepted: June 13, 2016 Published: June 23, 2016
OxLDL facilitate reactive oxygen species (ROS) formation and up-regulation of the executioner caspase-3 via the mitochondrial apoptotic pathway involves several critical steps in human endothelial cells. Previous studies reported that oxLDL-facilitated endothelial oxidative stress is associated with impairment of eNOS and up-regulation of inducible nitric oxide synthase (iNOS). Baicalein is the most abundant component that has anti-HIV, anti-tumor, anti-oxidant and free radical scavenging functions. In this present study, we shown that baicalein hinibits oxLDL-caused endothelial dysfunction through suppression of endothelial inflammation and oxidative stress that causes to cellular apoptosis. Specifically, baicalein reduces the elevation of ROS concentration, which subsequently inhibits the oxLDL-decreased expression of anti-oxidant enzymes, enriches the bioavailability of NO, stabilizes the mitochondrial membrane, thereby inhibiting the discharge of cytochrome c from mitochondria, a molecule required for the activation of the pro-apoptotic protein caspase 3. However, inhibition of eNOS impairs the anti-apoptotic and anti-inflammatory effects of baicalein. These results provide new insight into the possible molecular mechanisms by which baicalein protects against atherogenesis by NO-related pathways.
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