Evidence map›Paper›PMID 24400114›Full record

ArticlePloS one2014

Activation of the Nrf2/HO-1 antioxidant pathway contributes to the protective effects of Lycium barbarum polysaccharides in the rodent retina after ischemia-reperfusion-induced damage.

Meihua He, Hong Pan, Raymond Chuen-Chung Chang, Kwok-Fai So, Nicholas C Brecha, Mingliang Pu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
9.8field-weighted citation impact, top 1% 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

96 citing papers in PubMed, 195 citations in OpenAlex.

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36 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 3 countries.

Meihua HeDepartment of Anatomy/Embryology, School of Basic Medical Sciences, Peking University, Beijing, China ; Key Laboratory on Machine Perception (Ministry of Education), Peking University, Beijing, China ; Key Laboratory for Visual Impairment and Restoration (Ministry of Education), Peking University, Beijing, China.
Hong PanDepartment of Anatomy/Embryology, School of Basic Medical Sciences, Peking University, Beijing, China ; Key Laboratory on Machine Perception (Ministry of Education), Peking University, Beijing, China ; Key Laboratory for Visual Impairment and Restoration (Ministry of Education), Peking University, Beijing, China.
Raymond Chuen-Chung ChangDepartment of Anatomy and Research Center of Heart, Brain, Hormone and Healthy Aging, LKS Faculty of Medicine, Pokfulam, Hong Kong, China ; The State Key Laboratory of Brain and Cognitive Sciences, The University of Hong Kong, Pokfulam, Hong Kong, China.
Kwok-Fai SoDepartment of Anatomy and Research Center of Heart, Brain, Hormone and Healthy Aging, LKS Faculty of Medicine, Pokfulam, Hong Kong, China ; The State Key Laboratory of Brain and Cognitive Sciences, The University of Hong Kong, Pokfulam, Hong Kong, China ; GHM Institute of CNS Regeneration, Jinan University, Guangzhou, China.
Nicholas C BrechaDepartment of Ophthalmology, The University of Hong Kong, Pokfulam, Hong Kong, China ; Department of Neurobiology, Department of Medicine, Jules Stein Eye Institute, CURE Digestive Diseases Research Center, David Geffen School of Medicine at Los Angeles, University of California Los Angeles, Los Angeles, California, United States of America ; Veterans Administration, Greater Los Angeles Health System, Los Angeles, California, United States of America.
Mingliang PuDepartment of Anatomy/Embryology, School of Basic Medical Sciences, Peking University, Beijing, China ; Key Laboratory on Machine Perception (Ministry of Education), Peking University, Beijing, China ; Key Laboratory for Visual Impairment and Restoration (Ministry of Education), Peking University, Beijing, China.
Peking University · CNUniversity of Hong Kong · HK

Funding

NEUROCHEMICAL PATHWAYS IN THE INNER RETINAR01EY004067 · NEI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BRECHA, NICHOLAS C. · 1985 to 2019
$9.0M
Neurochemical Pathways in the Inner RetinaR56EY004067 · NEI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BRECHA, NICHOLAS C. · 2009 to 2009
$462k
BLRD VA I01 BX000764NEI NIH HHS EY04067NEI NIH HHS R01 EY004067NEI NIH HHS R56 EY004067
6 · The paper itself

Abstract

Lycium barbarum polysaccharides (LBP), extracts from the wolfberries, are protective to retina after ischemia-reperfusion (I/R). The antioxidant response element (ARE)-mediated antioxidant pathway plays an important role in maintaining the redox status of the retina. Heme oxygenase-1 (HO-1), combined with potent AREs in its promoter, is a highly effective therapeutic target for the protection against neurodegenerative diseases, including I/R-induced retinal damage. The aim of our present study was to investigate whether the protective effect of LBP after I/R damage was mediated via activation of the Nrf2/HO-1-antioxidant pathway in the retina. Retinal I/R was induced by an increase in intraocular pressure to 130 mm Hg for 60 minutes. Prior to the induction of ischemia, rats were orally treated with either vehicle (PBS) or LBP (1 mg/kg) once a day for 1 week. For specific experiments, zinc protoporphyrin (ZnPP, 20 mg/kg), an HO-1 inhibitor, was intraperitoneally administered at 24 h prior to ischemia. The protective effects of LBP were evaluated by quantifying ganglion cell and amacrine cell survival, and by measuring cell apoptosis in the retinal layers. In addition, HO-1 expression was examined using Western blotting and immunofluorescence analyses. Cytosolic and nuclear Nrf2 was measured using immunofluorescent staining. LBP treatment significantly increased Nrf2 nuclear accumulation and HO-1 expression in the retina after I/R injury. Increased apoptosis and a decrease in the number of viable cells were observed in the ganglion cell layer (GCL) and inner nuclear layer (INL) in the I/R retina, which were reversed by LBP treatment. The HO-1 inhibitor, ZnPP, diminished the LBP treatment-induced protective effects in the retina after I/R. Taken together, these results suggested that LBP partially exerted its beneficial neuroprotective effects via the activation of Nrf2 and an increase in HO-1 protein expression.

Indexed as

Amacrine CellsAnimalsApoptosisCell NucleusDisease Models, AnimalDrugs, Chinese HerbalEnzyme ActivationGene Expression RegulationHeme Oxygenase-1LyciumMaleNF-E2-Related Factor 2Oxidative StressProtein TransportRatsReactive Oxygen SpeciesDrugs, Chinese HerbalHeme Oxygenase-1lycium barbarum polysaccharideNF-E2-Related Factor 2Reactive Oxygen Species

Identifiers

PMID24400114
PMCPMC3882254
OpenAlexW2145071690

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.