Evidence map›Paper›PMID 27918469›Full record

ArticleNutrients2016

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

Min-Kyung Kang, Sin-Hye Park, Yun-Ho Kim, Eun-Jung Lee, Lucia Dwi Antika, Dong Yeon Kim, Yean-Jung Choi, Young-Hee Kang

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.0field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Molecular stress and neurovascular injury in the diabetic retina.The Journal of clinical investigation · 2026
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  10. Animal models of diabetic retinopathy.Annals of translational medicine · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Min-Kyung KangDepartment of Food Science and Nutrition, Hallym University, Chuncheon 24252, Korea. mitholy@hallym.ac.kr.
Sin-Hye ParkDepartment of Food Science and Nutrition, Hallym University, Chuncheon 24252, Korea. sinhyepark@hallym.ac.kr.
Yun-Ho KimDepartment of Food Science and Nutrition, Hallym University, Chuncheon 24252, Korea. royalskim@hallym.ac.kr.
Eun-Jung LeeDepartment of Food Science and Nutrition, Hallym University, Chuncheon 24252, Korea. reydmswjd@naver.com.
Lucia Dwi AntikaDepartment of Food Science and Nutrition, Hallym University, Chuncheon 24252, Korea. lucia.dwiantika@gmail.com.
Dong Yeon KimDepartment of Food Science and Nutrition, Hallym University, Chuncheon 24252, Korea. ehddus3290@naver.com.
Yean-Jung ChoiDepartment of Food Science and Nutrition, Hallym University, Chuncheon 24252, Korea. yjchoi79@hallym.ac.kr.
Young-Hee KangDepartment of Food Science and Nutrition, Hallym University, Chuncheon 24252, Korea. yhkang@hallym.ac.kr.
Hallym University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic retinopathy (DR) develops in a significant proportion of patients with chronic diabetes, characterized by retinal macular edema and abnormal retinal vessel outgrowth leading to vision loss. Chrysin, a naturally-occurring flavonoid found in herb and honeycomb, has anti-inflammatory, antioxidant, and anti-cancer properties. This study sought to determine the protective effects of chrysin on retinal neovascularization with abnormal vessels and blood-retinal barrier (BRB) breakdown in 33 mM glucose-exposed human retinal endothelial cells and in db/db mouse eyes. High glucose caused retinal endothelial apoptotic injury, which was inhibited by submicromolar chrysin. This compound diminished the enhanced induction of HIF-1α, vascular endothelial growth factor (VEGF), and VEGF receptor-2 (VEGFR2) in high glucose-exposed retinal endothelial cells. Consistently, oral administration of 10 mg/kg chrysin reduced the induction of these proteins in db/db mouse eye tissues. In addition, chrysin restored the decrement of VE-cadherin and ZO-1 junction proteins and PECAM-1 in hyperglycemia-stimulated retinal endothelial cells and diabetic mouse retina, possibly maintaining tight cell-cell interactions of endothelial cells and pericytes. Anti-apoptotic chrysin reduced the up-regulation of Ang-1, Ang-2, and Tie-2 crucial to retinal capillary occlusion and BRB permeability. Furthermore, orally treating chrysin inhibited acellular capillary formation, neovascularization, and vascular leakage observed in diabetic retinas. These observations demonstrate, for the first time, that chrysin had a capability to encumber diabetes-associated retinal neovascularization with microvascular abnormalities and BRB breakdown.

Indexed as

AnimalsAntigens, CDApoptosisCadherin 5CadherinsDiabetic RetinopathyFlavonoidsGlucoseHumansHyperglycemiaHypoxia-Inducible Factor 1, alpha SubunitMaleMiceMice, Inbred C57BLPlatelet Endothelial Cell Adhesion Molecule-1Receptor, TIE-2Ang2 protein, mouseangiogeninAntigens, CDCadherin 5CadherinschrysinFlavonoidsGlucoseHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitKdr protein, mousePlatelet Endothelial Cell Adhesion Molecule-1Receptor, TIE-2Ribonuclease, PancreaticTek protein, mouseTjp1 protein, mouseVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseVascular Endothelial Growth Factor Receptor-2Zonula Occludens-1 Proteinangiogenesisblood retinal barrierchrysindiabetic retinopathyretinal neovascularization

Identifiers

PMID27918469
PMCPMC5188437
OpenAlexW2560575531

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.