Quercetin protects against high glucose-induced damage in bone marrow-derived endothelial progenitor cells

Zhao, Leilei; Du, Yujun; Chen, Lei; Liu, Zhigang; Pan, Yuehai; Liu, Jianfeng; Liu, Bin

doi:10.3892/ijmm.2014.1852

Cited by 41 publications

(24 citation statements)

References 42 publications

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“…As expected, NAM efficiently inhibited the beneficial effect of quercetin on ROS scavenging, suggesting that the effect of quercetin on ROS clearance is SIRT-dependent. Recently, SIRT1, 2, and 3 were shown to be important for spindle organization and mitochondrial distribution in mouse oocytes [11, 12, 25, 27]. We also found that quercetin treatment reduced the frequency of spindle defects and altered the mitochondrial distribution, further supporting our conclusion that quercetin protects oocytes from postovulatory oocyte aging in a SIRT-dependent manner.…”

Section: Discussionsupporting

confidence: 88%

Quercetin delays postovulatory aging of mouse oocytes by regulating SIRT expression and MPF activity

Wang

et al. 2017

Oncotarget

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If no fertilization occurs at an appropriate time after ovulation, oocyte quality deteriorates rapidly as a process called postovulatory aging. Because the postovulatory aging of oocytes has detrimental effects on embryo development and offspring, many efforts have been made to prevent oocyte aging. Here we showed that quercetin prevented the decline in oocyte quality during postovulatory aging of oocytes. Quercetin treatment reduced aging-induced morphological changes and reactive oxygen species accumulation. Moreover, quercetin attenuated the aging-associated abnormalities in spindle organization and mitochondrial distribution, preventing decrease of SIRT expression and histone methylation. Quercetin also ameliorated the decrease in maturation-promoting factor activity and the onset of apoptosis during postovulatory aging. Furthermore, quercetin treatment during postovulatory aging improves early embryo development. Our results demonstrate that quercetin relieves deterioration in oocyte quality and improves subsequent embryo development.

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Section: Discussionsupporting

confidence: 88%

Quercetin delays postovulatory aging of mouse oocytes by regulating SIRT expression and MPF activity

Wang

et al. 2017

Oncotarget

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“…In vitro short-term exposure of EPCs to high-glucose, which impairs their number and functionality, determines SIRT1 downregulation, reduces FOXO1 deacetylation, and reduces eNOS phosphorylation (Fig. 4) (15,220). Consistent with these findings, in vitro and ex vivo studies demonstrate that poor glycemic control in type 2 diabetes patients reduces number of EPCs and differentiation capability by blocking SIRT1 signaling (3,17,116).…”

Section: Fig 4 Sirt1 and Sirt6 During Altered Glucose Homeostasis supporting

confidence: 53%

SIRT1 and SIRT6 Signaling Pathways in Cardiovascular Disease Protection

D’Onofrio¹,

Servillo²,

Balestrieri³

2018

Antioxidants & Redox Signaling

299

238

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Significance: Oxidative stress represents the common hallmark of pathological conditions associated with cardiovascular disease (CVD), including atherosclerosis, heart failure, hypertension, aging, diabetes, and other vascular system-related diseases. The sirtuin (SIRT) family, comprising seven proteins (SIRT1-SIRT7) sharing a highly conserved nicotinamide adenine dinucleotide (NAD + )-binding catalytic domain, attracted a great attention for the past few years as stress adaptor and epigenetic enzymes involved in the cellular events controlling aging-related disorder, cancer, and CVD. Recent Advances: Among sirtuins, SIRT1 and SIRT6 are the best characterized for their protective roles against inflammation, vascular aging, heart disease, and atherosclerotic plaque development. This latest role has been only recently unveiled for SIRT6. Of interest, in recent years, complex signaling networks controlled by SIRT1 and SIRT6 common to stress resistance, vascular aging, and CVD have emerged. Critical Issues: We provide a comprehensive overview of recent developments on the molecular signaling pathways controlled by SIRT1 and SIRT6, two post-translational modifiers proven to be valuable tools to dampen inflammation and oxidative stress at the cardiovascular level. Future Directions: A deeper understanding of the epigenetic mechanisms through which SIRT1 and SIRT6 act in the signalings responsible for onset and development CVD is a prime scientific endeavor of the upcoming years. Multiple ''omic'' technologies will have widespread implications in understanding such mechanisms, speeding up the achievement of selective and efficient pharmacological modulation of sirtuins for future applications in the prevention and treatment of CVD. Antioxid. Redox Signal. 28, 711-732.

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“…; Zhao et al . ). We found that SIRT1 protein abundance was increased 2.5‐ and 2.0‐fold in mdx and mdxQ, respectively, compared to C57.…”

Section: Resultsmentioning

confidence: 97%

Oral quercetin administration transiently protects respiratory function in dystrophin‐deficient mice

Selsby

Ballmann

Spaulding

et al. 2016

The Journal of Physiology

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Key pointr PGC-1α pathway activation has been shown to decrease disease severity and can be driven by quercetin.r Oral quercetin supplementation protected respiratory function for 4-6 months during a 12 month dosing regimen.r This transient protection was probably due to a failure to sustain elevated SIRT1 activity and downstream PGC-1α signalling.r Quercetin supplementation may be a beneficial treatment as part of a cocktail provided continued SIRT1 activity elevation is achieved.Abstract Duchenne muscular dystrophy (DMD) impacts 1 : 3500 boys and leads to muscle dysfunction culminating in death due to respiratory or cardiac failure. There is an urgent need for effective therapies with the potential for immediate application for this patient population. Quercetin, a flavonoid with an outstanding safety profile, may provide therapeutic relief to DMD patients as the wait for additional therapies continues. This study evaluated the capacity of orally administered quercetin (0.2%) in 2 month old mdx mice to improve respiratory function and end-point functional and histological outcomes in the diaphragm following 12 months of treatment. Respiratory function was protected for the first 4-6 months of treatment but appeared to become insensitive to quercetin thereafter. Consistent with this, end-point functional measures were decreased and histopathological measures were more severe in dystrophic muscle compared to C57 and similar between control-fed and quercetin-fed mdx mice. To better understand the transient nature of improved respiratory function, we measured PGC-1α pathway activity, which is suggested to be up-regulated by quercetin supplementation. This pathway was largely suppressed in dystrophic muscle compared to healthy muscle, and at the 14 month time point dietary quercetin enrichment did not increase expression of downstream effectors. These data support the efficacy of quercetin as an intervention for DMD in skeletal muscle, and also indicate the development of age-dependent quercetin insensitivity when continued supplementation fails to drive the PGC-1α pathway. Continued study is needed to determine if this is related to disease severity, age or other factors.

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Quercetin protects against high glucose-induced damage in bone marrow-derived endothelial progenitor cells

Cited by 41 publications

References 42 publications

Quercetin delays postovulatory aging of mouse oocytes by regulating SIRT expression and MPF activity

Quercetin delays postovulatory aging of mouse oocytes by regulating SIRT expression and MPF activity

SIRT1 and SIRT6 Signaling Pathways in Cardiovascular Disease Protection

Oral quercetin administration transiently protects respiratory function in dystrophin‐deficient mice

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