Quercetin Mitigates Inflammatory Responses Induced by Vascular Endothelial Growth Factor in Mouse Retinal Photoreceptor Cells through Suppression of Nuclear Factor Kappa B

Lee, Minsup; Yun, Seohyeon; Lee, Hyesook; Yang, Jong In

doi:10.3390/ijms18112497

Cited by 39 publications

(26 citation statements)

References 53 publications

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“…Moreover, we found that quercetin could suppress VCAM-1 expression in mouse aorta and cultured HUVECs ( Figure 3 , Figure 4 and Figure 5 ). This finding was consistent with that reported by Lee et al, showing that quercetin suppressed vascular endothelial growth factor-induced inflammatory responses, such as the translocation of nuclear factor kappa B, the upregulation of adhesion molecules and MMPs, and the downregulation of tight junction molecules [ 22 ]. In the present series of experiments, the tendency was shown that VCAM-1 expression in aorta tissue was lower in the quercetin treated sample than control sample.…”

Section: Discussionsupporting

confidence: 93%

Preventive Effects of Quercetin against the Onset of Atherosclerosis-Related Acute Aortic Syndromes in Mice

Kondo

Izawa‐Ishizawa

Goda

et al. 2020

IJMS

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Atherosclerosis-related acute aortic syndromes, such as aortic aneurysms or aortic dissection are life-threatening diseases. Since they develop suddenly and progress rapidly, the establishment of preventive strategies is urgently needed. Quercetin, a flavonoid abundant in various vegetables and fruits, is suggested to reduce the risk of cardiovascular disease. Therefore, in this study, the preventive effect of quercetin was evaluated using a mouse model of aortic aneurysm and dissection. The model was established by administering angiotensin II (Ang II) and β-aminopropionitrile (BAPN), a lysyl oxidase inhibitor, to mice to induce hypertension and degeneration of the elastic lamina, which would eventually result in the onset of an aortic aneurysm. Ang II, BAPN, and a nitric oxide synthase inhibitor was administered to induce aortic dissection via endothelial dysfunction. Quercetin (60 mg/kg/day) was administered 2 weeks before inducing aortic diseases by the end of the experiments (8 weeks in the aneurysm model, 6 weeks in the dissection model). It was found to reduce the incidence of aneurysm (from 72 to 45%), dissection (from 17 to 10%), and rupture (from 33 to 15%) in mice. Elastin degradation was ameliorated in the quercetin-treated mice compared to that in the mice without quercetin treatment (degradation score 2.9 ± 0.3 vs 2.2 ± 0.2). Furthermore, quercetin suppressed the expression of vascular cell adhesion molecule-1, macrophage infiltration, and pro-matrix metalloproteinase-9 activity. Our results suggest that quercetin might prevent the onset of atherosclerosis-related acute aortic syndromes through its anti-inflammatory and endothelial cell-protective effects.

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Section: Discussionsupporting

confidence: 93%

Preventive Effects of Quercetin against the Onset of Atherosclerosis-Related Acute Aortic Syndromes in Mice

Kondo

Izawa‐Ishizawa

Goda

et al. 2020

IJMS

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“…Ferulic acid, baicalein, coptisine, and wogonin downregulate NF-κB signaling ( Chen et al, 2017 ; Lampiasi and Montana, 2017 ; Shimizu et al, 2018 ), while berberine, catapol, and quercetin modulate PPAR-γ and NF-κB activities ( Le et al, 2015 ; Chuang et al, 2016 ; Li et al, 2016 ; Park, 2016 ; Wang Y.C. et al, 2016 ; Lee et al, 2017 ; Mahmoud et al, 2017 ). Additionally, pathway and functional enrichment analysis for putative targets revealed that DGLHD mainly regulated TNF-α, NF-κB, PPAR, and PI3K/Akt signaling pathway, which were all involved in fibrogenesis ( Seki and Schwabe, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

“…Importantly, baicalein, berberine, ferulic acid, catapol, coptisine and quercetin contained in DGLHD have been reported to exert anti-inflammatory and/or anti-fibrotic effects via inhibition of NF-κB pathway ( Sun et al, 2010 ; Le et al, 2015 ; Xu et al, 2015 ; Wang Y.C. et al, 2016 ; Chen et al, 2017 ; Lampiasi and Montana, 2017 ; Lee et al, 2017 ; Shimizu et al, 2018 ). Thereby, it seems reasonable that DGLHD repressed the development of fibrogenesis by modulating NF-κB activation.…”

Section: Discussionmentioning

confidence: 99%

Exploring the Mechanism of Dangguiliuhuang Decoction Against Hepatic Fibrosis by Network Pharmacology and Experimental Validation

Cao

Xie

et al. 2018

Front. Pharmacol.

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Dangguiliuhuang decoction (DGLHD) has been demonstrated to be effective in treating inflammatory, hepatic steatosis, and insulin resistance. In the study, we tried to elucidate the pharmacological efficacy and mechanism of DGLHD against liver fibrosis and predicate potential active ingredients and targets via network analysis and experimental validation. In the formula, we totally discovered 76 potential active ingredients like baicalein, berberine, and wogonin, and 286 corresponding targets including PTGS (prostaglandin-endoperoxide synthase) 2, PPAR (peroxisome proliferator-activated receptors) -γ, and NF-κB (nuclear factor-κB). Pathway and functional enrichment analysis of these putative targets indicated that DGLHD obviously influenced NF-κB and PPAR signaling pathway. Consistently, DGLHD downregulated levels of ALT (alanine transaminase) and AST (aspartate transaminase), reduced production of proinflammatory cytokines-TNF (tumor necrosis factor) -α and IL (Interleukin) -1β in serum and liver from mice with hepatic fibrosis, and inhibited hepatic stellate cell (HSC)-T6 cells proliferation. DGLHD decreased TGF (transforming growth factor) -β1 and α-SMA (smooth muscle actin) expression as well, maintained MMP (matrix metalloprotein) 13-TIMP (tissue inhibitor of metalloproteinases) 1 balance, leading to mitigated ECM (extracellular matrix) deposition in vivo and in vitro. Moreover, our experimental data confirmed that the alleviated inflammation and ECM accumulation were pertinent to NF-κB inhibition and PPAR-γ activation. Overall, our results suggest that DGLHD aims at multiply targets and impedes the progression of hepatic fibrosis by ameliorating abnormal inflammation and ECM deposition, thereby serving as a novel regimen for treating hepatic fibrosis in clinic.

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“…Oxidative stress activates host immune and other defense mechanisms that under prolonged insult exacerbate photoreceptor cell death by promoting exaggerated inflammatory responses (Kohno H et al, 2013, Rashid K et al, 2019. Flavonoids can inhibit the inflammatory reactions by suppressing the expression of pro-inflammatory genes and adhesion molecules implicated in the pathogenesis of retinal degeneration (Bian M et al, 2017, Cao X et al, 2010, Lee M et al, 2017. Indeed, bright light-induced retinal inflammation in Abca4 −/− Rdh8 −/− mice was remarkably suppressed by quercetin and myricetin, which at the molecular level correlated with the reduction of the expression of inflammatory markers.…”

Section: Downloaded Frommentioning

confidence: 99%

Protective Effects of Flavonoids in Acute Models of Light-Induced Retinal Degeneration

Ortega¹,

Parmar²,

Golczak³

et al. 2020

Mol Pharmacol

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Degeneration of photoreceptors caused by excessive illumination, inherited mutations or aging are the principal pathology of blinding diseases. Pharmacological compounds that stabilize the visual receptor, rhodopsin, and modulate the cellular pathways triggering death of photoreceptors could avert this pathology. Interestingly, flavonoids can modulate the cellular processes such as oxidative stress, inflammatory responses, and apoptosis that are activated during retinal degeneration. As we found previously, flavonoids also bind directly to unliganded rod opsin, enhancing its folding, stability, and regeneration. In addition, flavonoids stimulate rhodopsin gene expression. Thus, we evaluated the effect of two main dietary flavonoids, quercetin and myricetin in Abca4 −/− Rdh8 −/− and WT BALB/c mice susceptible to light-induced photoreceptors' degeneration. Using in vivo imaging such as optical coherence tomography, scanning laser ophthalmoscopy and histological assessment of retinal morphology, we found that treatment with these flavonoids prior to light insult remarkably protected retina from deterioration and preserved its function. Using HPLC-MS analysis, we detected these flavonoids in the eye upon their intraperitoneal administration. The molecular events associated with the protective effect of quercetin and myricetin were related to the elevated expression of photoreceptor-specific proteins, rhodopsin and cone opsins, decreased expression of the specific inflammatory markers, and the shift of the equilibrium between BAX/BCL-2 towards an anti-apoptotic profile. These results were confirmed in photoreceptor-derived 661W cells treated with either H 2 O 2 or all-trans-retinal stressors implicated in the mechanism of retinal degeneration. Altogether, flavonoids could have significant prophylactic value for retinal degenerative diseases.

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Quercetin Mitigates Inflammatory Responses Induced by Vascular Endothelial Growth Factor in Mouse Retinal Photoreceptor Cells through Suppression of Nuclear Factor Kappa B

Cited by 39 publications

References 53 publications

Preventive Effects of Quercetin against the Onset of Atherosclerosis-Related Acute Aortic Syndromes in Mice

Preventive Effects of Quercetin against the Onset of Atherosclerosis-Related Acute Aortic Syndromes in Mice

Exploring the Mechanism of Dangguiliuhuang Decoction Against Hepatic Fibrosis by Network Pharmacology and Experimental Validation

Protective Effects of Flavonoids in Acute Models of Light-Induced Retinal Degeneration

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