Chia Nan University of Pharmacy & Science Institutional Repository:Item 310902800/34750
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    Title: 紅藜與其活性成分對LED光源誘發視網膜傷害之保護效應
    The Protective Effect of Djulis and Its Bioactive Compounds against Light Emitting Diode Light-Induced Retina Damage, in Vitro and in Vivo
    Authors: 杜平惪
    Contributors: 食品科技系
    Keywords: 紅藜
    護眼效應
    發光二極體
    視網膜
    槲皮素
    甜菜鹼
    djulis
    eye protection
    liht emitting diode (LED)
    retina
    quercetin
    betanin.
    Date: 2022
    Issue Date: 2024-05-11 11:36:25 (UTC+8)
    Abstract: 國人接觸電子螢幕時間過長,尤其近年來3C產品充斥、螢幕鮮豔、亮度太高、使用時間過長等因素導致容易傷眼。因此,預防眼睛疾病乃為當務之急。其中藉由發掘天然活性物質以保護眼睛,是近年來的研究重點。現今有些廠商已關注到市場需求,惟受限於人力及研發等因素,有科學數據的相關護眼產品並不多。有鑑於此,本計畫「紅藜與其活性成分對LED光源誘發視網膜傷害之保護效應」之研發成果,可作為業界開發護眼機能產品之參考,尤其針對過度使用LED光源造成傷害之機能素材更值得發掘。一旦量產商品化,其市場競爭力將大為可觀。另在學術上可應用在教學與研究,在輔助醫療上也值得應用與參考。
    The aim of the first year proposal was to provide new insights into the role of the water extracts of Djulis (Chenopodium formosanum, WECF) and its bioactive compounds to prevent blue light (BL)-induced retinal damage in ARPE-19 cells. After 6 hours of BL exposure (peak at 450 nm), ARPE-19 cell viability significantly decreased, but treatment with water extract of djulis (WECF) at 0.1-25 µg/mL protected the cells from BL-induced phototoxicity. The cytoprotective effect of WECF were associated with a decrease in BL-induced oxidative stress and caspase-3 activity, and an increase in GSH levels and SOD activity. WECF also inhibited the expression of NF-κB protein and the MAPK signaling pathway, while upregulated heme oxygenase-1 (HO-1) via the Nrf2-mediated pathway. In addition, betanin, kaempferol, quercetin and rutin, presented in WECF, at 1-10 μM inhibited ROS generation and TBARS formation, and significantly restored GSH levels, increased SOD activity, and both kaempferol and quercetin at 10 μM significantly increased Nrf2 protein expression in the cell nucleus in blue light-induced AREP-19 cells, compared to the cells treated with blue light alone. Taken together, WECF and its bioactive compounds against blue light-induced retina damage, which could potentially be useful for treating retinal disease. In the second year of the study, an animal model was used as an experimental platform. The study aimed to investigate the effects of WECF, quercetin (Q) and betanin (B) on LED light-induced retinal damage in mice. The experimental design consisted of two models. In the first model, mice were initially exposed to LED light and subsequently administered the test substances. There were significant differences in superoxide dismutase (SOD) activity between the negative control group (NC) and mice treated with 10 mg/kg bw quercetin, 1.0 mg/kg bw betanin, 10 mg/kg bw betanin, and different concentrations (10, 50, 100 mg/kg bw) of WECF. However, no significant differences in TBARS in the eyeball, glutathione (GSH) content, or pathological changes in the inner nuclear layer (INL), outer nuclear layer (ONL), and inner and outer segments (IS&OS) thickness of the retina were found. Additionally, in model 2, where mice were first administered the test substances and then exposed to LED light, WECF (100 mg/kg bw) demonstrated superiority over NC in terms of antioxidant indices and pathological tissue changes, including ONL and IS&OS thickness. Quercetin excelled over NC in terms of GSH levels, inhibition of lipid oxidation, and IS&OS indices. Furthermore, low-concentration betanin outperformed NC in the IS&OS indices. Moreover, the administration of 300 mg/kg bw WECF significantly improved visual acuity (VA) and visual contrast sensitivity (VCS) compared to the negative control. Evaluation results from electroretinography (ERG) also indicated that the 300 mg/kg bw WECF had a protective effect on the retina. These findings suggest that pre-administration of WECF in mice demonstrated preventive effects against LED light-induced retinal damage. Overall, WECF and its bioactive components have been shown to protect retinal cells from blue light-induced damage. These findings are of significant reference value for the prevention of retinal diseases.
    Relation: 計畫編號:MOST110-2320-B041-001-MY2
    計畫年度:111
    計畫起訖:2022-08~2023-07
    Appears in Collections:[Dept. of Food Science & Technology] MOST Project

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