Dietary Compound Chrysin Inhibits Retinal Neovascularization with Abnormal Capillaries in db/db Mice

Kang, Min‐Kyung; Park, Sin‐Hye; Kim, Yun‐Ho; Lee, Eunjung; Antika, Lucia Dwi; Kim, Dong Yeon; Choi, Yong‐Kook; Kang, Young‐Hee

doi:10.3390/nu8120782

Cited by 22 publications

(26 citation statements)

References 45 publications

(100 reference statements)

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“…This study found that the treatment with micromolar chrysin reduced mesangial fibrosis through inhibiting collagen deposition and α-SMA induction in glucose-stimulated mesangial cells and in PAS-positive diabetic kidneys. Several studies have shown renorotection of chrysin in experimental animal models [ 30 , 40 , 41 , 42 , 43 ]. Our previous study revealed that chrysin dampened diabetes-associated renal tubulointerstitial fibrosis through inhibiting epithelial to mesenchymal transition [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

“…One study shows that serum angiopoietin-2 may be a potential predictor of acute pancreatitis severity and an indicator of renal dysfunction in the development of acute pancreatitis-renal syndrome [ 47 ]. Although this study did not monitor the serum angiopoietin-2 after chrysin treatment to diabetic mice, our previous study showed that oral administration of chrysin diminished the tissue level of angiopoietin-2 in diabetic mouse retina [ 30 ]. It was assumed that chrysin could modulate vessel outgrowth and sprouting leading to the promotion of angiogenesis and vasculogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…Our previous investigation showed that chrysin inhibited diabetes-associated renal tubulointerstitial fibrosis through blocking epithelial to mesenchymal transition [ 28 ] and ameliorated podocyte injury via an inhibition of endoplasmic reticulum stress [ 29 ]. Based on the possible anti-diabetic effects of chrysin [ 28 , 29 , 30 ], this study was designed to evaluate renoprotective potential of chrysin against diabetes-associated glomerulosclerosis in glucose- or bovine serum albumin-conjugated AGE (AGE-BSA)-exposed human renal mesangial cells (HRMC) and in db/db mice. The in vitro study demonstrated that the treatment with chrysin markedly suppressed mesangial fibrosis through blocking AGE-RAGE interaction and TGF-β signaling.…”

Section: Introductionmentioning

confidence: 99%

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Chrysin Inhibits Advanced Glycation End Products-Induced Kidney Fibrosis in Renal Mesangial Cells and Diabetic Kidneys

et al. 2018

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Advanced glycation end products (AGEs) play a causative role in the development of diabetic nephropathy via induction of matrix protein deposition in kidneys. This study investigated inhibitory effects of chrysin, present in bee propolis and herbs, on glomerulosclerosis in db/db mice and AGEs-exposed renal mesangial cells. The in vivo study explored the demoting effects of 10 mg/kg chrysin on glomerular fibrosis in a type 2 diabetic model. Oral supplementation of chrysin inhibited the collagen fiber accumulation and α-smooth muscle actin (α-SMA) induction in periodic acid schiff-positive renal tissues of db/db mice. Moreover, treating db/db mice with chrysin diminished the level of AGEs increased in diabetic glomeruli. The in vitro study employed human mesangial cells exposed to 100 μg/mL AGE-BSA for 72 h in the presence of 1–20 μM chrysin. Glucose increased mesangial AGE production via induction of receptor for AGEs. Chrysin suppressed the induction of collagens, α-SMA, fibroblast-specific protein-1 and matrix metalloproteinases enhanced by AGE-bovine serum albumin. Furthermore, chrysin blunted transforming growth factor-β1 induction and Smad 2/3 activation in AGEs-exposed mesangial cells. These results demonstrate that chrysin attenuated accumulation of myofibroblast-like cells and matrix proteins in AGEs-laden diabetic glomeruli. Therefore, chrysin may be a potential renoprotective agent targeting glucose-mediated AGEs-associated glomerulosclerosis and fibrosis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Chrysin Inhibits Advanced Glycation End Products-Induced Kidney Fibrosis in Renal Mesangial Cells and Diabetic Kidneys

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“…Following intake by humans, chrysin has low oral bioavailability and rapid fecal elimination, in which its major form in plasma is chrysin sulphate [ 28 , 30 ]. Our previous study showed that the multifunctional chrysin exerted the retinoprotection through inhibiting diabetes-associated retinal neovascularization and blood–retinal barrier breakdown [ 31 ]. However, whether chrysin is capable of preventing vision loss in diabetic ocular diseases remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Chrysin Ameliorates Malfunction of Retinoid Visual Cycle through Blocking Activation of AGE-RAGE-ER Stress in Glucose-Stimulated Retinal Pigment Epithelial Cells and Diabetic Eyes

et al. 2018

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Diabetes-associated visual cycle impairment has been implicated in diabetic retinopathy, and chronic hyperglycemia causes detrimental effects on visual function. Chrysin, a naturally occurring flavonoid found in various herbs, has anti-inflammatory, antioxidant, and neuroprotective properties. The goal of the current study was to identify the retinoprotective role of chrysin in maintaining robust retinoid visual cycle-related components. The in vitro study employed human retinal pigment epithelial (RPE) cells exposed to 33 mM of glucose or advanced glycation end products (AGEs) in the presence of 1–20 μM chrysin for three days. In the in vivo study, 10 mg/kg of chrysin was orally administrated to db/db mice. Treating chrysin reversed the glucose-induced production of vascular endothelial growth factor, insulin-like growth factor-1, and pigment epithelium-derived factor (PEDF) in RPE cells. The outer nuclear layer thickness of chrysin-exposed retina was enhanced. The oral gavage of chrysin augmented the levels of the visual cycle enzymes of RPE65, lecithin retinol acyltransferase (LRAT), retinol dehydrogenase 5 (RDH5), and rhodopsin diminished in db/db mouse retina. The diabetic tissue levels of the retinoid binding proteins and the receptor of the cellular retinol-binding protein, cellular retinaldehyde-binding protein-1, interphotoreceptor retinoid-binding protein and stimulated by retinoic acid 6 were restored to those of normal mouse retina. The presence of chrysin demoted AGE secretion and AGE receptor (RAGE) induction in glucose-exposed RPE cells and diabetic eyes. Chrysin inhibited the reduction of PEDF, RPE 65, LRAT, and RDH5 in 100 μg/mL of AGE-bovine serum albumin-exposed RPE cells. The treatment of RPE cells with chrysin reduced the activation of endoplasmic reticulum (ER) stress. Chrysin inhibited the impairment of the retinoid visual cycle through blocking ER stress via the AGE-RAGE activation in glucose-stimulated RPE cells and diabetic eyes. This is the first study demonstrating the protective effects of chrysin on the diabetes-associated malfunctioned visual cycle.

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“…At the same time, mRNA of tumor necrosis factor in vitreous body of patients and its expression of soluble receptors increased significantly. The animal research indicated that used angiogenin-1 could control the expression of tumor necrosis factor effectively, which was helpful to improve the prognosis of early diabetic retinopathy in rats [22][23][24].…”

Section: Discussionmentioning

confidence: 99%

The correlation between tumor necrosis factor gene polymorphism and diabetic retinopathy

Wang¹,

Wang²,

Jiang³

et al. 2018

biomedicalresearch

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Aim: Some studies showed that tumor necrosis factor gene polymorphism related to the progression of diabetes mellitus. The aim of this study is to explore the correlation between the gene polymorphism of tumor necrosis factor and diabetic retinopathy in clinical cases. Methods: We took the clinical cases as research subjects. The patients with type I and type II diabetes mellitus who had retinopathy and no retinopathy were 120 cases and 100 cases. At the same time, we analyzed gene polymorphism of tumor necrosis factor for all the patients (rs1800629). Results: A allelic gene of rs1800629 related to type I diabetes mellitus. We did not find significant correlation between rs1800629 and diabetic retinopathy by adjusting age, gender, duration of diabetes mellitus, HbALc, high blood pressure, kidney disease and other variables. Conclusion: This study has preliminarily confirmed that functional single nucleotide polymorphism A in promoter region related to type I diabetes mellitus, which had no significant correlation with diabetic retinopathy.

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Dietary Compound Chrysin Inhibits Retinal Neovascularization with Abnormal Capillaries in db/db Mice

Cited by 22 publications

References 45 publications

Chrysin Inhibits Advanced Glycation End Products-Induced Kidney Fibrosis in Renal Mesangial Cells and Diabetic Kidneys

Chrysin Inhibits Advanced Glycation End Products-Induced Kidney Fibrosis in Renal Mesangial Cells and Diabetic Kidneys

Chrysin Ameliorates Malfunction of Retinoid Visual Cycle through Blocking Activation of AGE-RAGE-ER Stress in Glucose-Stimulated Retinal Pigment Epithelial Cells and Diabetic Eyes

The correlation between tumor necrosis factor gene polymorphism and diabetic retinopathy

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