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Oncotarget 2017-Sep

Protective effect of resveratrol against light-induced retinal degeneration in aged SAMP8 mice.

Vain rekisteröityneet käyttäjät voivat kääntää artikkeleita
Kirjaudu sisään Rekisteröidy
Linkki tallennetaan leikepöydälle
Zhirong Liu
Zhengzheng Wu
Jie Li
Anna Marmalidou
Ruifan Zhang
Man Yu

Avainsanat

Abstrakti

OBJECTIVE

The purpose of this study was to determine the protective effects of Resveratrol (RESV) on acute bright light-induced retinal degeneration in aged senescence accelerated mouse strain.

METHODS

Ten three-month-old male SAMP8 mice (prone to aging) were randomly assigned to two experimental dietary groups: one untreated group and one RESV treatment group (n=20 eyes for each group). After 30 days of treatment, mice were exposed to intense bright light. Ten male SAMR1 mice (resistant to aging) served as control (n=20 eyes). The protective effects of RESV administration on light-induced retinal degeneration in SAMP8 strain as well as the effect of bright light damage in the retinas of SAMP8 mice were analyzed by electroretinography (ERG), retinal histology, mRNA, protein and lipid profile.

RESULTS

68%-85% of a-wave amplitude and 72%-92% of b-wave amplitude were persevered by RESV in SAMP8 mice that were exposed to light damage. Also, RESV preserved their photoreceptor nuclei. mRNA expression of neuroprotective factors leukemia inhibitory factor (LIF), brain derived neurotrophic factor (BDNF), oncostatin M (OSM), cardiotrophin 1(CT-1) and cardiotrophin-like cytokine (CLC) were up-regulated 28, 8, 7, 5 and 9-fold in SAMP8 mice after RESV treatment. In addition, RESV could suppress the NF-κB pathway by down-regulating the expression of pIκB. Light damage led to increase of saturated FA, monoenoic FA, n6 PUFA and n6/n3 ratio and decrease of Docosahexaenoic acid (DHA). There was no significant difference on DHA and the ratio of n6/n3-FA between the untreated and RESV treated SAMP8 mice.

CONCLUSIONS

Collectively, our study provides evidence that RESV prevents light-induced retinal damage associated with aging.

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