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Publications

Journal Article Epublish

PubMed: 40305267 DOI: 10.3390/biom15040523

Phlorizin Protects Against Oxidative Stress and Inflammation in Age-Related Macular Degeneration Model.

Biomolecules 15(4)

Authors: Zhen-Yu Liao, Chih-Yu Hung, Yu-Jou Hsu, I-Chia Liang, Yi-Chun Chen, Chao-Hsien Sung, Chi-Feng Hung

Affiliations

  • Department of Internal Medicine, Shin Kong Wu Ho-Su Memorial Hospital, Taipei 111, Taiwan.
  • Department of Ophthalmology, Chang Gung Memorial Hospital, Kweishan, Taoyuan 333, Taiwan.
  • PhD Program in Pharmaceutical Biotechnology, Fu Jen Catholic University, New Taipei City 242, Taiwan.
  • National Defense Medical Center, Department of Ophthalmology, Tri-Service General Hospital, Taipei 114, Taiwan.
  • Division of Anesthesiology, Fu Jen Catholic University Hospital, Fu Jen Catholic University, New Taipei City 242, Taiwan.
  • School of Medicine, Fu Jen Catholic University, New Taipei City 242, Taiwan.
  • School of Pharmacy, Kaohsiung Medical University, Kaohsiung 807, Taiwan.

Abstract

BACKGROUND

Sweet Tea (Lithocarpus polystachyus Rehd.), a traditional ethnobotanical medicine, contains phlorizin, a dihydrochalcone compound with antioxidative and anti-inflammatory properties. Given the critical role of oxidative stress and inflammation in age-related macular degeneration (AMD), this study tested the hypothesis that phlorizin mitigates oxidative damage and inflammation in AMD models, thereby offering therapeutic potential.

MATERIALS AND METHODS

Adult retinal pigmented epithelial cells (ARPE-19) were pre-treated with phlorizin (0.01-0.1 μM) and subjected to oxidative stress induced by ultraviolet A (UVA) radiation or sodium iodate (NaIO). Cell viability, reactive oxygen species (ROS) production, MAPK/NF-κB signaling, and the level of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and pro-angiogenic factors (VEGF, MMP2, MMP9) expression were assessed using MTT assays, fluorescence imaging, Western blotting, and RT-qPCR. In vivo, a laser-induced choroidal neovascularization (CNV) mouse model was used to evaluate phlorizin's effects on CNV formation and vascular leakage via fundus photography and fluorescence angiography.

RESULT

Phlorizin significantly enhanced cell viability, reduced ROS production, inhibited MAPK/NF-κB activation, and downregulated inflammatory and angiogenic mediators. In vivo studies confirmed the reduced CNV formation and vascular leakage following the phlorizin treatment.

CONCLUSIONS

Phlorizin demonstrated significant protective effects against oxidative stress and inflammation, highlighting its therapeutic potential for treating AMD.

MeSH

Macular Degeneration, Cells, Phlorhizin, Stress, Physiological, Oxidative Stress, Therapeutics