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Article: Long-term lutein administration attenuates retinal inflammation and functional deficits in early diabetic retinopathy using the Ins2Akita/+ mice

TitleLong-term lutein administration attenuates retinal inflammation and functional deficits in early diabetic retinopathy using the Ins2Akita/+ mice
Authors
Keywordsanimal cell
animal experiment
animal model
animal tissue
blood vessel function
Issue Date2020
PublisherBMJ Publishing Group: Open Access. The Journal's web site is located at http://drc.bmj.com/
Citation
BMJ Open Diabetes Research & Care, 2020, v. 8 n. 1, p. article no. e001519 How to Cite?
AbstractIntroduction Lutein is a carotenoid whose protective effects in the retina have been reported in various studies. The effect of lutein has not been reported in the retina of the Ins2Akita/+ mouse, a well-characterized genetic model for diabetic retinopathy (DR) in which the etiology of diabetes is better defined than the chemically induced diabetes. The objective of the present study is to investigate the effect of long-term administration of lutein in early stages of DR using the Ins2Akita/+ mouse. Research design and methods Heterozygous male Ins2Akita/+ and age-matched wild-type mice were used. Lutein was administered to the mice in drinking water starting 6 weeks old daily until analysis at 4.5, 6.5 or 9 months of age. Plain water served as non-treatment control. Microglia were immunostained with ionized calcium-binding adapter molecule 1 (Iba-1) and cluster of differentiation 68 (CD68) in retinal flat-mounts. Vascular endothelial growth factor (VEGF) level in the retina was assessed by enzyme-linked immunosorbent assay (ELISA). Vascular permeability was analyzed in retinal flat-mounts after fluorescein isothiocyanate (FITC)-dextran perfusion. Retinal occludin expression was assessed via Western blots. Retinal function was examined by electroretinography (ERG). Results Increased microglial reactivity was detected in the Ins2Akita/+ mouse retina and was suppressed by lutein. Lutein administration also reduced the upregulation of VEGF in the Ins2Akita/+ mouse retina. Increased vascular leakage and decreased occludin expression were observed in the Ins2Akita/+ mouse retina, and these alterations were attenuated by lutein treatment. ERG recordings showed reduced a-wave and b-wave amplitudes in the Ins2Akita/+ mice. With lutein treatment, the ERG deficits were significantly alleviated. Conclusions We showed beneficial effects of long-term lutein administration in the Ins2Akita/+ mouse retina, including suppression of retinal inflammation, protection of retinal vasculature and preservation of retinal function. These results point to lutein’s potential as a long-term therapeutic intervention for prevention of inflammation and retinal degeneration in patients with early DR.
Persistent Identifierhttp://hdl.handle.net/10722/287922
ISSN
2018 Impact Factor: 5.067
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorWANG, W-
dc.contributor.authorTam, KC-
dc.contributor.authorNg, TC-
dc.contributor.authorGOIT, RK-
dc.contributor.authorChan, KLS-
dc.contributor.authorLo, ACY-
dc.date.accessioned2020-10-05T12:05:12Z-
dc.date.available2020-10-05T12:05:12Z-
dc.date.issued2020-
dc.identifier.citationBMJ Open Diabetes Research & Care, 2020, v. 8 n. 1, p. article no. e001519-
dc.identifier.issn2052-4897-
dc.identifier.urihttp://hdl.handle.net/10722/287922-
dc.description.abstractIntroduction Lutein is a carotenoid whose protective effects in the retina have been reported in various studies. The effect of lutein has not been reported in the retina of the Ins2Akita/+ mouse, a well-characterized genetic model for diabetic retinopathy (DR) in which the etiology of diabetes is better defined than the chemically induced diabetes. The objective of the present study is to investigate the effect of long-term administration of lutein in early stages of DR using the Ins2Akita/+ mouse. Research design and methods Heterozygous male Ins2Akita/+ and age-matched wild-type mice were used. Lutein was administered to the mice in drinking water starting 6 weeks old daily until analysis at 4.5, 6.5 or 9 months of age. Plain water served as non-treatment control. Microglia were immunostained with ionized calcium-binding adapter molecule 1 (Iba-1) and cluster of differentiation 68 (CD68) in retinal flat-mounts. Vascular endothelial growth factor (VEGF) level in the retina was assessed by enzyme-linked immunosorbent assay (ELISA). Vascular permeability was analyzed in retinal flat-mounts after fluorescein isothiocyanate (FITC)-dextran perfusion. Retinal occludin expression was assessed via Western blots. Retinal function was examined by electroretinography (ERG). Results Increased microglial reactivity was detected in the Ins2Akita/+ mouse retina and was suppressed by lutein. Lutein administration also reduced the upregulation of VEGF in the Ins2Akita/+ mouse retina. Increased vascular leakage and decreased occludin expression were observed in the Ins2Akita/+ mouse retina, and these alterations were attenuated by lutein treatment. ERG recordings showed reduced a-wave and b-wave amplitudes in the Ins2Akita/+ mice. With lutein treatment, the ERG deficits were significantly alleviated. Conclusions We showed beneficial effects of long-term lutein administration in the Ins2Akita/+ mouse retina, including suppression of retinal inflammation, protection of retinal vasculature and preservation of retinal function. These results point to lutein’s potential as a long-term therapeutic intervention for prevention of inflammation and retinal degeneration in patients with early DR.-
dc.languageeng-
dc.publisherBMJ Publishing Group: Open Access. The Journal's web site is located at http://drc.bmj.com/-
dc.relation.ispartofBMJ Open Diabetes Research & Care-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectanimal cell-
dc.subjectanimal experiment-
dc.subjectanimal model-
dc.subjectanimal tissue-
dc.subjectblood vessel function-
dc.titleLong-term lutein administration attenuates retinal inflammation and functional deficits in early diabetic retinopathy using the Ins2Akita/+ mice-
dc.typeArticle-
dc.identifier.emailTam, KC: bkctam@hku.hk-
dc.identifier.emailNg, TC: dngtc@hku.hk-
dc.identifier.emailLo, ACY: amylo@hku.hk-
dc.identifier.authorityLo, ACY=rp00425-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1136/bmjdrc-2020-001519-
dc.identifier.pmid32665315-
dc.identifier.pmcidPMC7365433-
dc.identifier.scopuseid_2-s2.0-85088010251-
dc.identifier.hkuros314719-
dc.identifier.volume8-
dc.identifier.issue1-
dc.identifier.spagearticle no. e001519-
dc.identifier.epagearticle no. e001519-
dc.publisher.placeUnited Kingdom-

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