Long-term oral administration of naringenin counteracts aging-related retinal degeneration via regulation of mitochondrial dynamics and autophagy

Aging-related retinal degeneration can manifest as decreased visual function due to damage to retinal structures and dysfunction in retinal homeostasis. Naringenin, a flavonoid, has beneficial effects in preventing cellular aging, preserving the functionality of photoreceptors, and slowing down visu...

Full description

Bibliographic Details
Main Authors: Guiping Chen, Ling Zeng, Feng Yan, Jinlong Liu, Mengqi Qin, Feifei Wang, Xu Zhang
Format: Article
Language:English
Published: Frontiers Media S.A. 2022-07-01
Series:Frontiers in Pharmacology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fphar.2022.919905/full
_version_ 1811296766558994432
author Guiping Chen
Ling Zeng
Feng Yan
Feng Yan
Jinlong Liu
Mengqi Qin
Feifei Wang
Xu Zhang
author_facet Guiping Chen
Ling Zeng
Feng Yan
Feng Yan
Jinlong Liu
Mengqi Qin
Feifei Wang
Xu Zhang
author_sort Guiping Chen
collection DOAJ
description Aging-related retinal degeneration can manifest as decreased visual function due to damage to retinal structures and dysfunction in retinal homeostasis. Naringenin, a flavonoid, has beneficial effects in preventing cellular aging, preserving the functionality of photoreceptors, and slowing down visual function loss. However, the role and potential mechanism of naringenin in the aging mouse retina require further investigation. In this study, we evaluated the effects of naringenin on the aging eye using electroretinogram (ERG) and hematoxylin and eosin staining and explored its potential mechanism by western blotting. ERG showed that naringenin increased the amplitude of the a- and b-waves of scotopic 3.0, 10.0, and the a-wave amplitude of photopic 3.0 in the aging mouse retina. Furthermore, administration of naringenin prevented aging-induced retinal degeneration in the total retina, ganglion cell, inner plexiform layer, inner nuclear layer, and outer nuclear layer. The expression of mitochondrial fusion protein two was increased, OPA1 protein expression and the ratio of L-OPA1/S-OPA1 were unchanged, and dynamin-related protein one was decreased in the 12-month-old mice treated with naringenin compared with the 12-month-old mice treated with vehicle. Furthermore, the downregulation of age-related alterations in autophagy was significantly rescued in the aging mice by treatment with naringenin. Taken together, these results suggest that the oral administration of naringenin improves visual function, retinal structure, mitochondrial dynamics, and autophagy in the aging mouse retinas. Naringenin may be a potential dietary supplement for the prevention or treatment of aging-related retinal degeneration.
first_indexed 2024-04-13T05:54:23Z
format Article
id doaj.art-b113ac597cf14442b7a4c0197742a370
institution Directory Open Access Journal
issn 1663-9812
language English
last_indexed 2024-04-13T05:54:23Z
publishDate 2022-07-01
publisher Frontiers Media S.A.
record_format Article
series Frontiers in Pharmacology
spelling doaj.art-b113ac597cf14442b7a4c0197742a3702022-12-22T02:59:41ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122022-07-011310.3389/fphar.2022.919905919905Long-term oral administration of naringenin counteracts aging-related retinal degeneration via regulation of mitochondrial dynamics and autophagyGuiping Chen0Ling Zeng1Feng Yan2Feng Yan3Jinlong Liu4Mengqi Qin5Feifei Wang6Xu Zhang7Affiliated Eye Hospital of Nanchang University, Jiangxi Clinical Research Center of Ophthalmic Disease, Jiangxi Provincial Key Laboratory for Ophthalmology, Nanchang, JX, ChinaAffiliated Eye Hospital of Nanchang University, Jiangxi Clinical Research Center of Ophthalmic Disease, Jiangxi Provincial Key Laboratory for Ophthalmology, Nanchang, JX, ChinaAffiliated Eye Hospital of Nanchang University, Jiangxi Clinical Research Center of Ophthalmic Disease, Jiangxi Provincial Key Laboratory for Ophthalmology, Nanchang, JX, ChinaSchool of Pharmacy, Nanchang University, Nanchang, JX, ChinaAffiliated Eye Hospital of Nanchang University, Jiangxi Clinical Research Center of Ophthalmic Disease, Jiangxi Provincial Key Laboratory for Ophthalmology, Nanchang, JX, ChinaAffiliated Eye Hospital of Nanchang University, Jiangxi Clinical Research Center of Ophthalmic Disease, Jiangxi Provincial Key Laboratory for Ophthalmology, Nanchang, JX, ChinaAffiliated Eye Hospital of Nanchang University, Jiangxi Clinical Research Center of Ophthalmic Disease, Jiangxi Provincial Key Laboratory for Ophthalmology, Nanchang, JX, ChinaAffiliated Eye Hospital of Nanchang University, Jiangxi Clinical Research Center of Ophthalmic Disease, Jiangxi Provincial Key Laboratory for Ophthalmology, Nanchang, JX, ChinaAging-related retinal degeneration can manifest as decreased visual function due to damage to retinal structures and dysfunction in retinal homeostasis. Naringenin, a flavonoid, has beneficial effects in preventing cellular aging, preserving the functionality of photoreceptors, and slowing down visual function loss. However, the role and potential mechanism of naringenin in the aging mouse retina require further investigation. In this study, we evaluated the effects of naringenin on the aging eye using electroretinogram (ERG) and hematoxylin and eosin staining and explored its potential mechanism by western blotting. ERG showed that naringenin increased the amplitude of the a- and b-waves of scotopic 3.0, 10.0, and the a-wave amplitude of photopic 3.0 in the aging mouse retina. Furthermore, administration of naringenin prevented aging-induced retinal degeneration in the total retina, ganglion cell, inner plexiform layer, inner nuclear layer, and outer nuclear layer. The expression of mitochondrial fusion protein two was increased, OPA1 protein expression and the ratio of L-OPA1/S-OPA1 were unchanged, and dynamin-related protein one was decreased in the 12-month-old mice treated with naringenin compared with the 12-month-old mice treated with vehicle. Furthermore, the downregulation of age-related alterations in autophagy was significantly rescued in the aging mice by treatment with naringenin. Taken together, these results suggest that the oral administration of naringenin improves visual function, retinal structure, mitochondrial dynamics, and autophagy in the aging mouse retinas. Naringenin may be a potential dietary supplement for the prevention or treatment of aging-related retinal degeneration.https://www.frontiersin.org/articles/10.3389/fphar.2022.919905/fullnaringeninaging eyevisual functionmitochondria dynamicsautophagy
spellingShingle Guiping Chen
Ling Zeng
Feng Yan
Feng Yan
Jinlong Liu
Mengqi Qin
Feifei Wang
Xu Zhang
Long-term oral administration of naringenin counteracts aging-related retinal degeneration via regulation of mitochondrial dynamics and autophagy
Frontiers in Pharmacology
naringenin
aging eye
visual function
mitochondria dynamics
autophagy
title Long-term oral administration of naringenin counteracts aging-related retinal degeneration via regulation of mitochondrial dynamics and autophagy
title_full Long-term oral administration of naringenin counteracts aging-related retinal degeneration via regulation of mitochondrial dynamics and autophagy
title_fullStr Long-term oral administration of naringenin counteracts aging-related retinal degeneration via regulation of mitochondrial dynamics and autophagy
title_full_unstemmed Long-term oral administration of naringenin counteracts aging-related retinal degeneration via regulation of mitochondrial dynamics and autophagy
title_short Long-term oral administration of naringenin counteracts aging-related retinal degeneration via regulation of mitochondrial dynamics and autophagy
title_sort long term oral administration of naringenin counteracts aging related retinal degeneration via regulation of mitochondrial dynamics and autophagy
topic naringenin
aging eye
visual function
mitochondria dynamics
autophagy
url https://www.frontiersin.org/articles/10.3389/fphar.2022.919905/full
work_keys_str_mv AT guipingchen longtermoraladministrationofnaringenincounteractsagingrelatedretinaldegenerationviaregulationofmitochondrialdynamicsandautophagy
AT lingzeng longtermoraladministrationofnaringenincounteractsagingrelatedretinaldegenerationviaregulationofmitochondrialdynamicsandautophagy
AT fengyan longtermoraladministrationofnaringenincounteractsagingrelatedretinaldegenerationviaregulationofmitochondrialdynamicsandautophagy
AT fengyan longtermoraladministrationofnaringenincounteractsagingrelatedretinaldegenerationviaregulationofmitochondrialdynamicsandautophagy
AT jinlongliu longtermoraladministrationofnaringenincounteractsagingrelatedretinaldegenerationviaregulationofmitochondrialdynamicsandautophagy
AT mengqiqin longtermoraladministrationofnaringenincounteractsagingrelatedretinaldegenerationviaregulationofmitochondrialdynamicsandautophagy
AT feifeiwang longtermoraladministrationofnaringenincounteractsagingrelatedretinaldegenerationviaregulationofmitochondrialdynamicsandautophagy
AT xuzhang longtermoraladministrationofnaringenincounteractsagingrelatedretinaldegenerationviaregulationofmitochondrialdynamicsandautophagy