Evidence map›Paper›PMID 38504533›Full record

ArticleJournal of traditional Chinese medicine = Chung i tsa chih ying wen pan2024

Emodin suppresses alkali burn-induced corneal inflammation and neovascularization by the vascular endothelial growth factor receptor 2 signaling pathway.

Zheng Xueying, Guo Liang, Lai Siyi, L I Fengyue, Liang Mingli, Liu Wanting, Meng Chun, Liu Guanghui

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.2field-weighted citation impact, top 18% 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

4 citing papers in PubMed, 2 citations in OpenAlex.

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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 2 institutions in 1 country.

Zheng XueyingDepartment of Bioengineering, College of Biological Science and Biotechnology, Fuzhou University, Fuzhou 350104, China.
Guo LiangDepartment of Bioengineering, College of Biological Science and Biotechnology, Fuzhou University, Fuzhou 350104, China.
Lai SiyiDepartment of Ophthalmology, Affiliated People's Hospital (Fujian Provincial People's Hospital), Fujian University of Traditional Chinese Medicine, Fuzhou 350004, China.
L I FengyueDepartment of Bioengineering, College of Biological Science and Biotechnology, Fuzhou University, Fuzhou 350104, China.
Liang MingliDepartment of Bioengineering, College of Biological Science and Biotechnology, Fuzhou University, Fuzhou 350104, China.
Liu WantingDepartment of Bioengineering, College of Biological Science and Biotechnology, Fuzhou University, Fuzhou 350104, China.
Meng ChunDepartment of Bioengineering, College of Biological Science and Biotechnology, Fuzhou University, Fuzhou 350104, China.
Liu GuanghuiDepartment of Ophthalmology, Affiliated People's Hospital (Fujian Provincial People's Hospital), Fujian University of Traditional Chinese Medicine, Fuzhou 350004, China.
Fujian Provincial People's Hospital · CNFujian University of Traditional Chinese Medicine · CN

Funding

Fujian Major Research Grants for Young and Middle-aged Health Professionals(Research and Development of Anti-Keratitis Protein Drug Sgp130) 2021ZQNZD012National Natural Science Foundation of China(Study on Mechanism of Yijing Decoction in Preventing Microvascular Damage of Early Diabetic Retinopathy based on MMPs/TIMPs) 81774369
6 · The paper itself

Abstract

objectiveTo investigate the effects of emodin on alkali burn-induced corneal inflammation and neovascularization.

methodsThe ability of emodin to target vascular endothelial growth factor receptor 2 (VEGFR2) was predicted by molecular docking. The effects of emodin on the invasion, migration, and proliferation of human umbilical vein endothelial cells (HUVEC) were determined by cell counting kit-8, Transwell, and tube formation assays. Analysis of apoptosis was performed by flow cytometry. CD31 levels were examined by immunofluorescence. The abundance and phosphorylation state of VEGFR2, protein kinase B (Akt), signal transducer and activator of transcription 3 (STAT3), and P38 were examined by immunoblot analysis. Corneal alkali burn was performed on 40 mice. Animals were divided randomly into two groups, and the alkali-burned eyes were then treated with drops of either 10 μM emodin or phosphate buffered saline (PBS) four times a day. Slit-lamp microscopy was used to evaluate inflammation and corneal neovascularization (CNV) in all eyes on Days 0, 7, 10, and 14. The mice were killed humanely 14 d after the alkali burn, and their corneas were removed and preserved at －80 ℃ until histological study or protein extraction.

resultsMolecular docking confirmed that emodin was able to target VEGFR2. The findings revealed that emodin decreased the invasion, migration, angiogenesis, and proliferation of HUVEC in a dose-dependent manner. In mice, emodin suppressed corneal inflammatory cell infiltration and inhibited the development of corneal neovascularization induced by alkali burn. Compared to those of the PBS-treated group, lower VEGFR2 expression and CD31 levels were found in the emodin-treated group. Emodin dramatically decreased the expression of VEGFR2, p-VEGFR2, p-Akt, p-STAT3, and p-P38 in VEGF-treated HUVEC.

conclusionThis study provides a new avenue for evaluating the molecular mechanisms underlying corneal inflammation and neovascularization. Emodin might be a promising new therapeutic option for corneal alkali burns.

Indexed as

Burns, ChemicalCorneal NeovascularizationEmodinAnimalsDisease Models, AnimalHumansHuman Umbilical Vein Endothelial CellsInflammationMiceMolecular Docking SimulationNeovascularization, PathologicProto-Oncogene Proteins c-aktSignal TransductionVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2EmodinProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2alkali burncorneal inflammationcorneal neovascularisationemodinsignal transductionvascular endothelial growth factor receptor-2

Identifiers

PMID38504533
PMCPMC10927407
OpenAlexW4394738912

What OpenQuestion holds

Textmetadata
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.