Quercetin alleviates 4-hydroxynonenal-induced cytotoxicity and inflammation in ARPE-19 cells

Hytti, Maria; Piippo, Niina; Salminen, Antero; Honkakoski, Paavo; Kaarniranta, Kai; Kauppinen, Anu

doi:10.1016/j.exer.2015.02.001

Cited by 51 publications

(35 citation statements)

References 41 publications

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“…The effects of UPARANT on the levels of transcription factors involved in CNV [3][4][5]23 were investigated. As displayed in Figure 5, laser treatment increased the levels of HIF-1a by approximately 4.2-fold (P < 0.001) and enhanced the phosphorylation of STAT3 at Tyr 705 , NF-kB p65 at both Ser 276 and Ser 536 , and CREB at Ser 133 by approximately 28.6-, 6.1-, 4.4-, and 3.3-fold, respectively (P < 0.001).…”

Section: Uparant Downregulates Levels Of Transcription Factorsmentioning

confidence: 99%

“…T he leading cause for vision loss in the Western world is attributed to age-related macular degeneration (AMD), 1 of which neovascular AMD (nAMD) affects nearly two thirds of advanced AMD patients. 2 The imbalance in a multitude of angiogenic and inflammatory factors, under the control of hypoxia-dependent and -independent transcription factors, [3][4][5] leads to choroidal neovascularization (CNV) with invasion of the subretinal space by the newly formed vessels and leakage from the choroid. 3 Retinal pigment epithelium plays a primary role in maintaining the outer blood retinal barrier (oBRB), and RPE cells are a major source of angiogenic and inflammatory factors.…”

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confidence: 99%

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The Urokinase Receptor-Derived Peptide UPARANT Mitigates Angiogenesis in a Mouse Model of Laser-Induced Choroidal Neovascularization

Cammalleri

Monte

Locri

et al. 2016

Invest. Ophthalmol. Vis. Sci.

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Section: Uparant Downregulates Levels Of Transcription Factorsmentioning

confidence: 99%

mentioning

confidence: 99%

The Urokinase Receptor-Derived Peptide UPARANT Mitigates Angiogenesis in a Mouse Model of Laser-Induced Choroidal Neovascularization

Cammalleri

Monte

Locri

et al. 2016

Invest. Ophthalmol. Vis. Sci.

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“…In the retina, we found that Qcn protected ARPE-19 cells from oxidative stress injury [14]. Other studies reported that Qcn has protective effects in the retina ischemia-reperfusion injury [15], ocular inflammation [16], and neuroprotective effects on RGC in glaucoma [17]. However, whether Qcn protects the RGCs in rAION is poorly understood.…”

Section: Introductionmentioning

confidence: 80%

“…The current results demonstrated that Qcn decreased the expression of ED-1 and Iba-1, i.e., decreased the extrinsic macrophage and resident microglia infiltration in ONs. Qcn treatment has also been reported to stabilize the blood-retinal barrier and prevent inflammation in diabetic rat retina and ARPE-19 cells [15,23]. Notably, Qcn exhibits the potential to stabilize the blood-ON barrier and restrict the infiltration of the inflammatory response at the ischemic ONs.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of quercetin in a rodent model of anterior ischemic optic neuropathy (rAION)

Lyu

Min

Gong

et al. 2019

Preprint

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Background: Anterior ischemic optic neuropathy (AION) is the leading cause of sudden optic nerve-related (ON-related) vision loss in elderly people. However, no considerable treatments are available for the neuroprotection of NAION. The purpose of this study was to detect the effects of intravitreal injection of quercetin (Qcn) in a rodent model of anterior ischemic optic neuropathy (rAION). Methods: The rAION model was established using verteporfin and laser in a photodynamic procedure on the optic discs (ON) of rats. The rats received intravitreal injection of Qcn 2 days before the injury and once/week for 4 weeks after the infarct on optic neuropathy. Flash-visual evoked potential (VEP) were recorded to assess the visual function. TUNEL and retrograde Fluorogold labeling assessed the apoptosis and density of retinal ganglion cells (RGCs). ED-1 and Iba-1 staining of the optic nerves displayed the inflammatory response. Results: At 14 days post-infarct, Qcn treatment significantly reduced the number of apoptotic RGCs, as well as, ED1/Iba-1-positive cells/high power field(HPF) in the ON (p<0.01) as compared to the rAION group. At week 4 after rAION, 28.4% VEP amplitudes were estimated in the treated eyes of the fellow eyes in the rAION group and 64.7% in the rAION+Qcn group (p<0.01). In addition, Qcn saved the RGCs in the central retinas as compared to those of the rAION group (1967.5±162.1 and 2868±325.3 mm2, respectively (p<0.01), and the corresponding densities were 1654.8±104.8 and 2208±272.9 mm2 in the mid-peripheral retinas, respectively (p<0.01). Conclusion: The intravitreal injection of Qcn could protect the RGCs from injury in the rAION animal model, as demonstrated anatomically by RGC density and functionally by F-VEP. Moreover, Qcn might exert an anti-apoptosis role in the survival of RGCs and anti-inflammatory in the optic nerves.

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“…In human adult retinal pigmented epithelial (ARPE-19) cells, cyanidin-3-glucoside protects against 4-HNE-induced cell apoptosis, inflammatory damage, and angiogenesis [12,57]. Quercetin also increases viability and decreases inflammation and cytotoxicity in 4-HNE-exposed ARPE-19 cells [58]. Recently, solid dispersion of quercetin has been reported to decrease retinal pigment epithelium sediments and Bruch's membrane thickness in Nrf2 wild-type (WT) mice with dry age-related macular degeneration.…”

Section: Prevention Of Eye Damagementioning

confidence: 99%

Can Medicinal Plants and Bioactive Compounds Combat Lipid Peroxidation Product 4-HNE-Induced Deleterious Effects?

Wang

et al. 2020

Biomolecules

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The toxic reactive aldehyde 4-hydroxynonenal (4-HNE) belongs to the advanced lipid peroxidation end products. Accumulation of 4-HNE and formation of 4-HNE adducts induced by redox imbalance participate in several cytotoxic processes, which contribute to the pathogenesis and progression of oxidative stress-related human disorders. Medicinal plants and bioactive natural compounds are suggested to be attractive sources of potential agents to mitigate oxidative stress, but little is known about the therapeutic potentials especially on combating 4-HNE-induced deleterious effects. Of note, some investigations clarify the attenuation of medicinal plants and bioactive compounds on 4-HNE-induced disturbances, but strong evidence is needed that these plants and compounds serve as potent agents in the prevention and treatment of disorders driven by 4-HNE. Therefore, this review highlights the pharmacological basis of these medicinal plants and bioactive compounds to combat 4-HNE-induced deleterious effects in oxidative stress-related disorders, such as neurotoxicity and neurological disorder, eye damage, cardiovascular injury, liver injury, and energy metabolism disorder. In addition, this review briefly discusses with special attention to the strategies for developing potential therapies by future applications of these medicinal plants and bioactive compounds, which will help biological and pharmacological scientists to explore the new vistas of medicinal plants in combating 4-HNE-induced deleterious effects.

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Quercetin alleviates 4-hydroxynonenal-induced cytotoxicity and inflammation in ARPE-19 cells

Cited by 51 publications

References 41 publications

The Urokinase Receptor-Derived Peptide UPARANT Mitigates Angiogenesis in a Mouse Model of Laser-Induced Choroidal Neovascularization

The Urokinase Receptor-Derived Peptide UPARANT Mitigates Angiogenesis in a Mouse Model of Laser-Induced Choroidal Neovascularization

Protective effects of quercetin in a rodent model of anterior ischemic optic neuropathy (rAION)

Can Medicinal Plants and Bioactive Compounds Combat Lipid Peroxidation Product 4-HNE-Induced Deleterious Effects?

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