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Published on: December 11, 2020
Fructus lycii mitigates oxidative stress in dry age-related macular degeneration models via Nrf2/ARE pathway
Yuan Peng1, Ling-Yan Liang2, Han-Lei Wei1
1Department of Ophthalmology, Affiliated Hospital of Jiangxi University of Traditional Chinese Medicine, Nanchang 330006, Jiangxi Province, China.
Aim:
To evaluate the effect of Fructus lycii (FL) aqueous extract on dry age-related macular degeneration (AMD) in mice via the nuclear factor erythroid 2-related factor 2/antioxidant response element (Nrf2/ARE) signaling pathway and investigate the protective effect of FL-containing serum on hydrogen peroxide (H2O2)-treated human retinal pigment epithelial cells (ARPE-19) in vitro.
Methods:
In vivo dry AMD mouse model was established by intraperitoneal injection of NaIO3 solution and treated with aqueous extract of FL. The pathological changes of mouse retinal tissues were observed by electron microscopy; the activity of superoxide dismutase (SOD) and catalase (CAT) in mouse serum was detected by colorimetric method. In vitro dry AMD model was established by H2O2 induction of ARPE-19 cells and treated with FL-containing serum. Methylthiazolyldiphenyl-tetrazolium bromide assay and scratch assay were performed to detect cell activity and proliferation ability. Expression of Nrf2, heme oxygenase-1 (HO-1), and glutamate-cysteine ligase catalytic subunit (GCLC) in retinal tissues and ARPE-19 cells were detected by Western blot and quantitative real-time polymerase chain reaction (Q-PCR).
Results:
The in vivo study revealed severe deposits under the retinal pigment epithelium and thickened Bruch's membrane in dry AMD mice. However, aqueous extract of FL reduced the formation of deposits and decreased the thickness of Bruch's membrane. SOD and CAT activities were significantly reduced in the serum of dry AMD mice, and aqueous extract of FL upregulated SOD and CAT activities. In addition, gene and protein expression of Nrf2, HO-1, and GCLC were significantly downregulated in dry AMD mice, but significantly upregulated by FL aqueous extract treatment. In vitro studies showed that H2O2 inhibited the activity and proliferative capacity of ARPE-19 cells and downregulated the protein and gene expression of Nrf2, HO-1 and GCLC. However, in H2O2-treated ARPE-19 cells, FL-containing serum not only increased cell activity and proliferative capacity, but also upregulated protein and gene expression of Nrf2, HO-1, and GCLC.
Conclusion:
FL reduces oxidative stress in an animal model of dry AMD through the Nrf2/ARE signaling pathway and has a protective effect on dry AMD in vitro and in vivo, providing new insights into the therapeutic use of FL for dry AMD.
Insights
Fructus lycii (FL) extract reduces oxidative stress in dry age-related macular degeneration (AMD) mouse models by activating the Nrf2/ARE pathway. FL demonstrates protective effects on retinal cells, suggesting therapeutic potential for dry AMD.
Area of Science:
- Ophthalmology
- Pharmacology
- Cell Biology
Background:
- Dry age-related macular degeneration (AMD) is a leading cause of vision loss.
- Oxidative stress plays a critical role in the pathogenesis of dry AMD.
- The Nrf2/ARE signaling pathway is a key regulator of cellular antioxidant defense.
Purpose of the Study:
- To evaluate the therapeutic effect of Fructus lycii (FL) aqueous extract on dry AMD in mice.
- To investigate the role of the Nrf2/ARE signaling pathway in FL's protective mechanism.
- To assess the protective effects of FL-containing serum on human retinal pigment epithelial cells (ARPE-19) in vitro.
Main Methods:
- Established dry AMD mouse models using NaIO3 and treated with FL extract.
- Assessed retinal pathology via electron microscopy and measured serum antioxidant enzyme activity (SOD, CAT).
- Utilized hydrogen peroxide (H2O2) to induce dry AMD in ARPE-19 cells, treated with FL-containing serum, and analyzed cell viability, proliferation, and Nrf2/ARE pathway gene/protein expression (Nrf2, HO-1, GCLC) via Western blot and Q-PCR.
Main Results:
- FL extract reduced retinal deposits and Bruch's membrane thickening in dry AMD mice.
- FL treatment significantly upregulated SOD and CAT activities and enhanced Nrf2, HO-1, and GCLC expression in vivo.
- In vitro, FL-containing serum protected ARPE-19 cells from H2O2-induced damage, improving cell activity and proliferation while upregulating Nrf2/ARE pathway components.
Conclusions:
- Fructus lycii aqueous extract mitigates oxidative stress in a dry AMD mouse model via the Nrf2/ARE signaling pathway.
- FL exhibits protective effects against dry AMD both in vivo and in vitro.
- FL shows promise as a therapeutic agent for dry AMD, warranting further investigation.