scholarly journals Angelica sinensis has inherent endothelial cell toxicity at high concentrations but can also protect the vascular endothelium from oxidative stress-induced injury at moderate concentrations

2011 ◽  
Vol 1 (1) ◽  
pp. 8
Author(s):  
Miko Yamada ◽  
Betty Pat ◽  
Glenda Gobe ◽  
Ken Wojcikowski
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Heme Oxygenase ◽  
Angelica Sinensis ◽  
Molecular Characteristics ◽  
Heme Oxygenase 1 ◽  
High Concentrations ◽  
Induced Apoptosis ◽  
And Oxidative Stress

Hypoxia and oxidative stress are important factors in the pathogenesis of many acute forms of injury, especially acute kidney injury. Apoptosis is a key mode of endothelial cell death from oxidative stress. Minimising the detrimental effects of oxidative stress is necessary to reduce injury, and new treatment strategies are constantly being sought. The aim of this study was to investigate the ability of an aqueous/methanol extract of Angelica sinensis (AS) root (Chinese names Danggui, Dong quai, Donggui) to protect endothelium from hypoxia and oxidative stress. This was compared in specialised kidney endothelium (renal medullary vascular endothelial cells; RMVEC) versus central endothelium (aortic endothelial cells; AEC). Toxicity of various strengths of AS was first tested in RMVEC and AEC using % apoptosis and mitosis as outcomes. Morphological and molecular characteristics of apoptosis and mitosis, and the effect of AS on heme-oxygenase-1, a marker of cellular response to oxidative stress, were also investigated. The results showed that, at concentrations of 2500µg/mL or greater, AS significantly increased apoptosis in RMVEC and AEC (P<0.05), however concentrations of 2000 µg/mL or less were non-toxic and also non-mitogenic. Endothelial cells were then treated with hydrogen peroxide (0.8 mM for RMVEC; 0.6 mM for AEC) for oxidative stress, with and without 2000 µg/mL AS. AS significantly inhibited oxidant-induced apoptosis (P<0.05) but had little effect on mitosis. AS also increased heme-oxygenase-1, but only in AEC. AS extracts may have some inherent toxicity at high concentrations, but with careful analysis of non-toxic levels, both renal and central endothelium benefited from AS against oxidative stress-induced apoptosis, without inducing excessive mitosis, and AS may find application in some oxidant-induced disease.

Resveratrol increases vascular oxidative stress resistance

2007 ◽  
Vol 292 (5) ◽  
pp. H2417-H2424 ◽  
Author(s):  
Zoltan Ungvari ◽  
Zsuzsanna Orosz ◽  
Aracelie Rivera ◽  
Nazar Labinskyy ◽  
Zhao Xiangmin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Cell Death ◽  
Endothelial Cell ◽  
Glutathione Peroxidase ◽  
Heme Oxygenase ◽  
Stress Resistance ◽  
Heme Oxygenase 1 ◽  
Resveratrol Treatment ◽  
Vascular Oxidative Stress

Epidemiological studies suggest that Mediterranean diets rich in resveratrol are associated with reduced risk of coronary artery disease. However, the mechanisms by which resveratrol exerts its vasculoprotective effects are not completely understood. Because oxidative stress and endothelial cell injury play a critical role in vascular aging and atherogenesis, we evaluated whether resveratrol inhibits oxidative stress-induced endothelial apoptosis. We found that oxidized LDL and TNF-α elicited significant increases in caspase-3/7 activity in endothelial cells and cultured rat aortas, which were prevented by resveratrol pretreatment (10−6–10−4 mol/l). The protective effect of resveratrol was attenuated by inhibition of glutathione peroxidase and heme oxygenase-1, suggesting a role for antioxidant systems in the antiapoptotic action of resveratrol. Indeed, resveratrol treatment protected cultured aortic segments and/or endothelial cells against increases in intracellular H2O2 levels and H2O2-mediated apoptotic cell death induced by oxidative stressors (exogenous H2O2, paraquat, and UV light). Resveratrol treatment also attenuated UV-induced DNA damage (comet assay). Resveratrol treatment upregulated the expression of glutathione peroxidase, catalase, and heme oxygenase-1 in cultured arteries, whereas it had no significant effect on the expression of SOD isoforms. Resveratrol also effectively scavenged H2O2 in vitro. Thus resveratrol seems to increase vascular oxidative stress resistance by scavenging H2O2 and preventing oxidative stress-induced endothelial cell death. We propose that the antioxidant and antiapoptotic effects of resveratrol, together with its previously described anti-inflammatory actions, are responsible, at least in part, for its cardioprotective effects.

scholarly journals Epigallocatechin Gallate Attenuates Proliferation and Oxidative Stress in Human Vascular Smooth Muscle Cells Induced by Interleukin-1βvia Heme Oxygenase-1

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Po-Len Liu ◽  
Jung-Tung Liu ◽  
Hsuan-Fu Kuo ◽  
Inn-Wen Chong ◽  
Chong-Chao Hsieh
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Green Tea ◽  
Vascular Smooth Muscle Cells ◽  
Heme Oxygenase ◽  
Muscle Cells ◽  
Heme Oxygenase 1 ◽  
And Oxidative Stress

Proliferation of vascular smooth muscle cells (VSMCs) triggered by inflammatory stimuli and oxidative stress contributes importantly to atherogenesis. The association of green tea consumption with cardiovascular protection has been well documented in epidemiological observations, however, the underlying mechanisms remain unclear. This study aimed to elucidate the effects of the most active green tea catechin derivative, (−)-epigallocatechin-3-gallate (EGCG), in human aortic smooth muscle cells (HASMCs), focusing particularly on the role of a potent anti-inflammatory and antioxidative enzyme heme oxygenase-1 (HO-1). We found that pretreatment of EGCG dose- and time-dependently induced HO-1 protein levels in HASMCs. EGCG inhibited interleukin- (IL-)1β-induced HASMC proliferation and oxidative stress in a dose-dependent manner. The HO-1 inducer CoPPIX decreased IL-1β-induced cell proliferation, whereas the HO-1 enzyme inhibitor ZnPPIX significantly reversed EGCG-caused growth inhibition in IL-1β-treated HASMCs. At the molecular level, EGCG treatment significantly activated nuclear factor erythroid-2-related factor (Nrf2) transcription activities. These results suggest that EGCG might serve as a complementary and alternative medicine in the treatment of these pathologies by inducing HO-1 expression and subsequently decreasing VSMC proliferation.

scholarly journals Oxidative stress causes enhanced endothelial cell injury in human heme oxygenase-1 deficiency

1999 ◽  
Vol 103 (1) ◽  
pp. 129-135 ◽  
Author(s):  
Akihiro Yachie ◽  
Yo Niida ◽  
Taizo Wada ◽  
Noboru Igarashi ◽  
Hisashi Kaneda ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cell ◽  
Heme Oxygenase ◽  
Cell Injury ◽  
Heme Oxygenase 1 ◽  
Endothelial Cell Injury
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