Differential suppression of intracellular reactive oxygen species-mediated signaling pathway in vascular endothelial cells by several subclasses of flavonoids

Lv, Yi; Chen, Chun-Ye; Jin, Xin; Zhang, Ting; Zhou, Yong; Zhang, Qianyong; Zhu, Jingjing; Mi, Mantian

doi:10.1016/j.biochi.2012.05.027

Cited by 69 publications

(50 citation statements)

References 49 publications

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“…Although suppression of MMP-9 expression by kaempferol, quercetin, and morin was reported in different conditions Lee et al, 2013;Lin et al, 2010;Sivaramakrishnan and Niranjali Devaraj, 2009;Yi et al, 2012), our study showed that MMP-9 secretion from HT-1080 cells was severely decreased by galangin as well as kaempferol, and moderately decreased by fisetin. Interestingly, quercetin weakly affected and morin did not affect MMP-9 secretion.…”

Section: Discussioncontrasting

confidence: 55%

Galangin and Kaempferol Suppress Phorbol-12-Myristate-13-Acetate-Induced Matrix Metalloproteinase-9 Expression in Human Fibrosarcoma HT-1080 Cells

Choi¹,

Lee²,

Lee³

2015

Molecules and Cells

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Matrix metalloproteinase (MMP)-9 degrades type IV collagen in the basement membrane and plays crucial roles in several pathological implications, including tumorigenesis and inflammation. In this study, we analyzed the effect of flavonols on MMP-9 expression in phorbol-12-myristate-13-acetate (PMA)-induced human fibrosarcoma HT-1080 cells. Galangin and kaempferol efficiently decreased MMP-9 secretion, whereas fisetin only weakly decreased its secretion. Galangin and kaempferol did not affect cell viability at concentrations up to 30 M. Luciferase reporter assays showed that galangin and kaempferol decrease transcription of MMP-9 mRNA. Moreover, galangin and kaempferol strongly reduce IB phosphorylation and significantly decrease JNK phosphorylation. These results indicate that galangin and kaempferol suppress PMA-induced MMP-9 expression by blocking activation of NF-B and AP-1. Therefore, these flavonols could be used as chemopreventive agents to lower the risk of diseases involving MMP-9.

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Section: Discussioncontrasting

confidence: 55%

Galangin and Kaempferol Suppress Phorbol-12-Myristate-13-Acetate-Induced Matrix Metalloproteinase-9 Expression in Human Fibrosarcoma HT-1080 Cells

Choi¹,

Lee²,

Lee³

2015

Molecules and Cells

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“…[22][23][24] In this study, we attempted to clarify whether some flavonoids have the ability to suppress CoCl 2 -elicited decreases in EC-SOD. Among the 7 flavonoids examined in the present study (Fig.…”

Section: Effects Of Flavonoids On Cocl 2 -Elicited Decreases In Ec-sodmentioning

confidence: 99%

“…[22][23][24] We previously reported that luteolin significantly suppressed phorbol ester (TPA)-induced human monocytic differentiation into macrophages, and these events were closely associated with the inhibition of intracellular ROS signaling. 25) Accordingly, some flavonoids may be seed compounds that maintain redox homeostasis.…”

mentioning

confidence: 99%

CoCl<sub>2</sub> Decreases EC-SOD Expression through Histone Deacetylation in COS7 Cells

Hattori

Kamiya

Hara

et al. 2016

Biological & Pharmaceutical Bulletin

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Extracellular-superoxide dismutase (EC-SOD), one of the SOD isozymes, is negatively regulated under hypoxic conditions, and decreases in its expression may exacerbate vascular diseases. Moreover, epigenetics, such as DNA methylation and histone modifications, are known to play a critical role in the progression of cancer, type 2 diabetes, and atherosclerosis. We previously investigated the involvement of reactive oxygen species (ROS) and p38 mitogen-activated protein kinase (MAPK) in decreases in EC-SOD expression in hypoxic COS7 cells; however, the role of epigenetics in this process currently remains unknown. In the present study, we demonstrated that the hypoxia mimetic cobalt chloride (CoCl 2 ) decreased histone acetylation levels, and a pretreatment with 4-phenyl butyric acid (PBA), an inhibitor of histone deacetylase, significantly suppressed CoCl 2 -elicited histone deacetylation and decreases in EC-SOD. We found that CoCl 2 -elicited decreases in EC-SOD were accompanied by reductions in histone H3 acetylation levels within its promoter region. Furthermore, luteolin, a well-known flavonoid, significantly suppressed the CoCl 2 -elicited accumulation of ROS, p38-MAPK activation, and histone deacetylation. Collectively, the results of the present study showed for the first time that CoCl 2 decreases the expression of EC-SOD through its deacetylation and luteolin may be one of the seed compounds that maintain redox homeostasis, even under hypoxic conditions.

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“…The cardiovascular protective effects of the natural product quercetin, such as its antioxidant 19, anti‐inflammatory 20 and possible promotion of cholesterol efflux effects 21, have attracted a great deal of attention. We assumed that the coupling of quercetin and N ‐acetylneuraminic acid (the major form of sialic acid in mammalians) 16, 17, 18, 22, 23 could not only enhance the cardiovascular protective functions of quercetin but also protect biomolecules against desialylation.…”

Section: Introductionmentioning

confidence: 99%

Synthesis and cardiovascular protective effects of quercetin 7‐O‐sialic acid

Tian

Liu

Qin

et al. 2016

J Cellular Molecular Medi

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Oxidative stress and inflammation play important roles in the pathogenesis of cardiovascular disease (CVD). Oxidative stress‐induced desialylation is considered to be a primary step in atherogenic modification, and therefore, the attenuation of oxidative stress and/or inflammatory reactions may ameliorate CVD. In this study, quercetin 7‐O‐sialic acid (QA) was synthesized aiming to put together the cardiovascular protective effect of quercetin and the recently reported anti‐oxidant and anti‐atherosclerosis functions of N‐acetylneuraminic acid. The biological efficacy of QA was evaluated in vitro in various cellular models. The results demonstrated that 50 μM QA could effectively protect human umbilical vein endothelial cells (HUVEC, EA.hy926) against hydrogen peroxide‐ or oxidized low‐density lipoprotein‐induced oxidative damage by reducing the production of reactive oxygen species. QA attenuated hydrogen peroxide‐induced desialylation of HUVEC and lipoproteins. QA decreased lipopolysaccharide‐induced secretion of tumour necrosis factor‐α (TNF‐α) and monocyte chemoattractant protein‐1 (MCP‐1), and it significantly reduced the expression of intercellular adhesion molecule‐1, vascular cell adhesion molecule‐1, TNF‐α and MCP‐1. Furthermore, QA effectively promoted cholesterol efflux from Raw 264.7 macrophages to apolipoprotein A‐1 and high‐density lipoprotein by up‐regulating ATP‐binding cassette transporter A1 and G1, respectively. Results indicated that the novel compound QA exhibited a better capacity than quercetin for anti‐oxidation, anti‐inflammation, cholesterol efflux promotion and biomolecule protection against desialylation and therefore could be a candidate compound for the prevention or treatment of CVD.

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Differential suppression of intracellular reactive oxygen species-mediated signaling pathway in vascular endothelial cells by several subclasses of flavonoids

Cited by 69 publications

References 49 publications

Galangin and Kaempferol Suppress Phorbol-12-Myristate-13-Acetate-Induced Matrix Metalloproteinase-9 Expression in Human Fibrosarcoma HT-1080 Cells

Galangin and Kaempferol Suppress Phorbol-12-Myristate-13-Acetate-Induced Matrix Metalloproteinase-9 Expression in Human Fibrosarcoma HT-1080 Cells

CoCl<sub>2</sub> Decreases EC-SOD Expression through Histone Deacetylation in COS7 Cells

Synthesis and cardiovascular protective effects of quercetin 7‐O‐sialic acid

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