Baicalein is an available anti-atherosclerotic compound through modulation of nitric oxide-related mechanism under oxLDL exposure

Shih Hung Chan, Ching Hsia Hung, Jhih Yuan Shih, Pei Ming Chu, Yung Hsin Cheng, Yi Ju Tsai, Huei Chen Lin, Kun Ling Tsai

研究成果: Article

5 引文 (Scopus)

摘要

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 oxLDLfacilitated 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.

原文English
頁(從 - 到)42881-42891
頁數11
期刊Oncotarget
7
發行號28
DOIs
出版狀態Published - 2016 一月 1

指紋

Nitric Oxide
Oxidants
Caspase 3
Reactive Oxygen Species
Oxidative Stress
Up-Regulation
Apoptosis Regulatory Proteins
Mitochondrial Membranes
Nitric Oxide Synthase Type II
Cytochromes c
Biological Availability
Free Radicals
Atherosclerosis
Mitochondria
Anti-Inflammatory Agents
Endothelial Cells
baicalein
oxidized low density lipoprotein
HIV
Apoptosis

All Science Journal Classification (ASJC) codes

  • Oncology

引用此文

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title = "Baicalein is an available anti-atherosclerotic compound through modulation of nitric oxide-related mechanism under oxLDL exposure",
abstract = "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 oxLDLfacilitated 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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Baicalein is an available anti-atherosclerotic compound through modulation of nitric oxide-related mechanism under oxLDL exposure. / Chan, Shih Hung; Hung, Ching Hsia; Shih, Jhih Yuan; Chu, Pei Ming; Cheng, Yung Hsin; Tsai, Yi Ju; Lin, Huei Chen; Tsai, Kun Ling.

於: Oncotarget, 卷 7, 編號 28, 01.01.2016, p. 42881-42891.

研究成果: Article

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AU - Chan, Shih Hung

AU - Hung, Ching Hsia

AU - Shih, Jhih Yuan

AU - Chu, Pei Ming

AU - Cheng, Yung Hsin

AU - Tsai, Yi Ju

AU - Lin, Huei Chen

AU - Tsai, Kun Ling

PY - 2016/1/1

Y1 - 2016/1/1

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