• 한방안이비인후피부과학회지
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• 제28권3호
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• pp.66-75
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• 2015

Object : The purpose of this study is to understand age-related maculardegeneration(AMD) with both western and Korean medicine.Methods : We investigated the comprehension of general AMD degenation in both western and Korean medicine through literature review.Results : The results are as follows.1. AMD prevalent increasing as the population ages; however, treatment options remain limited and incompletely defined.2. Generally macular degeneration has been affected by aging and is associate with the function of kidney(腎) and liver(肝) in Korean medicine.Conclusion : Further studies are needed to apply comprehension of AMD in Korean medicine to clinical stage.

• 약학회지
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• 제56권5호
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• pp.314-319
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• 2012

Age-related macular degeneration (AMD) is the leading cause of vision loss and blindness among the elderly. In this study, extract of Vaccinium uliginosum L. that has potent antioxidant activity was evaluated as effective preventive supplement for AMD using AMD animal model induced by high fat diet and UV A irradiation. Treatment with VU extract protected photoreceptor cells of retina and blocked the accumulation of lipofuscin pigment-granules induced by high fat diet and UV A light irradiation. This study suggests that VU extract may be a useful agent for prevention of progress of AMD.

• BMB Reports
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• 제47권5호
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• pp.292-297
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• 2014

Age-related macular degeneration (AMD) is the leading cause of blindness in the world. Evidence indicates that the suppression of the ubiquitin-proteasome system (UPS) contributes to the accumulation of toxic proteins and inflammation in retinal pigment epithelium (RPE), the functional abnormalities and/or the degeneration of which are believed to be the initiators and major pathologies of AMD. To identify new protein associations with the altered UPS in AMD, we used LC-ESI-MS/MS to perform a proteomic analysis of the aqueous humor (AH) of AMD patients and matched control subjects. Six UPS-related proteins were present in the AH of the patients and control subjects. Four of the proteins, including 26S proteasome non-ATPase regulatory subunit 1 (Rpn2), were increased in patients, according to semi-quantitative proteomic profiling. An LC-MRM assay revealed a significant increase of Rpn2 in 15 AMD patients compared to the control subjects, suggesting that this protein could be a biomarker for AMD.

• Biomolecules & Therapeutics
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• 제30권3호
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• pp.291-297
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• 2022

Dry age-related macular degeneration (AMD) is a type of progressive blindness that is primarily due to dysfunction and the loss of retinal pigment epithelium (RPE). The accumulation of N-retinylidene-N-retinylethanolamine (A2E), a by-product of the visual cycle, causes RPE and photoreceptor degeneration that impairs vision. Genes associated with dry AMD have been identified using a blue light model of A2E accumulation in the retinal pigment epithelium and transcriptomic studies of retinal tissue from patients with AMD. However, dry macular degeneration progresses slowly, and current approaches cannot reveal changes in gene transcription according to stages of AMD progression. Thus, they are limited in terms of identifying genes responsible for pathogenesis. Here, we created a model of long-term exposure to identify temporally-dependent changes in gene expression induced in human retinal pigment epithelial cells (ARPE-19) exposed to blue light and a non-cytotoxic dose of A2E for 120 days. We identified stage-specific genes at 40, 100, and 120 days, respectively. The expression of genes corresponding to epithelial-mesenchymal transition (EMT) during the early stage, glycolysis and angiogenesis during the middle stage, and apoptosis and inflammation pathways during the late stage was significantly altered by A2E and blue light. Changes in the expression of genes at the late stages of the EMT were similar to those found in human eyes with late-stage AMD. Our results provide further insight into the pathogenesis of dry AMD induced by blue light and a novel model in vitro with which relevant genes can be identified in the future.

• 디지털융복합연구
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• 제19권10호
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• pp.535-543
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• 2021

노인성 안질환과 구강질환은 비가역적 손상을 일으키기 때문에 삶의 질에 큰 영향을 미친다. 따라서 나이관련황반변성(AMD) 및 녹내장과 같은 노인성 안질환과 구강건강행태와의 관련성을 확인하고자 하였다. 제7기 2차년도(2017) 국민건강영양조사 자료를 이용하여 AMD 및 녹내장과 구강건강행태를 분석하였다. 녹내장과 AMD 유병자와 녹내장과 AMD 미보유자를 비교하기 위해 교차분석을 실시하였고, 복합로지스틱 회귀분석을 통해 AMD 및 녹내장과 구강건강행태와의 위험비를 확인하였다. 황반변성 및 녹내장의 유무에 따라 연령, 학력, 구강위생용품 사용, 발음불편 호소에서 통계적으로 유의한 차이가 있었다. 또한 녹내장 유무는 성별에서도 차이가 있었다. 구강건강행태와 노인성 안질환과의 일부 변수에서 유의한 연관성이 있었다. 구강건강행태는 AMD 및 녹내장 질환을 예방하는 데 위험 요인으로 작용할 수 있으므로 구강건강행태에 대한 인식도가 더욱 높아져야 할 것이다.

• 한국멀티미디어학회논문지
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• 제20권8호
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• pp.1291-1298
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• 2017

Optical coherence tomography (OCT) is the most common medical imaging device with the ability to image the retina in eyes at micrometer resolution and to visualize the pathological indicators of many retinal diseases such as Age-Related Macular Degeneration (AMD) and diabetic retinopathy. Accordingly, there have been research activities to analyze and process OCT images to identify those indicators and make medical decisions based on the findings. In this paper, we use a deep convolutional neural network for analysis of OCT volume data to distinguish AMD from normal patients. We propose a novel approach where images in each OCT volume are grouped together into sub-volumes and the network is trained by those sub-volumes instead of individual images. We conducted an experiment using public data set to evaluate the performance of the proposed approach. The experiment confirmed performance improvement of our approach over the traditional image-by-image training approach.

• Journal of Ginseng Research
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• 제47권1호
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• pp.65-73
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• 2023

Background: Age-related macular degeneration (AMD) is a significant visual disease that induces impaired vision and irreversible blindness in the elderly. However, the effects of ginseng berry extract (GBE) on the retina have not been studied. Therefore, this study aimed to investigate the protective effects of GBE on blue light (BL)-induced retinal damage and elucidate its underlying mechanisms in human retinal pigment epithelial cells (ARPE-19 cells) and Balb/c retina. Methods: To investigate the effects and underlying mechanisms of GBE on retinal damage in vitro, we performed cell viability assay, pre-and post-treatment of sample, reactive oxygen species (ROS) assay, quantitative real-time PCR (qRT-PCR), and western immunoblotting using A2E-laden ARPE-19 cells with BL exposure. In addition, Balb/c mice were irradiated with BL to induce retinal degeneration and orally administrated with GBE (50, 100, 200 mg/kg). Using the harvested retina, we performed histological analysis (thickness of retinal layers), qRT-PCR, and western immunoblotting to elucidate the effects and mechanisms of GBE against retinal damage in vivo. Results: GBE significantly inhibited BL-induced cell damage in ARPE-19 cells by activating the SIRT1/PGC-1α pathway, regulating NF-kB translocation, caspase 3 activation, PARP cleavage, expressions of apoptosis-related factors (BAX/BCL-2, LC3-II, and p62), and ROS production. Furthermore, GBE prevented BL-induced retinal degeneration by restoring the thickness of retinal layers and suppressed inflammation and apoptosis via regulation of NF-kB and SIRT1/PGC-1α pathway, cleavage of caspase 3 and PARP, and expressions of apoptosis-related factors in vivo. Conclusions: GBE could be a potential agent to prevent dry AMD and progression to wet AMD.

• BMB Reports
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• 제48권9호
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• pp.525-530
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• 2015

Activation of the Wnt/β-catenin pathway plays a pathogenic role in age-related macular degeneration (AMD) and is thus a potential target for the development of therapeutics for this disease. Here, we demonstrated that Wnt5a antagonized β-catenin response transcription (CRT) induced with Wnt3a by promoting β-catenin phosphorylation at Ser33/Ser37/Thr41 and its subsequent degradation in human retinal pigment epithelial (RPE) cells. Wnt5a decreased the levels of vascular endothelial growth factor (VEGF), tumor necrosis factor-α(TNF-α), and nuclear factor-κB (NF-κB), which was up-regulated by Wnt3a. Furthermore, Wnt5a increased E-cadherin expression and decreased cell migration by down-regulating Snail expression, thereby abrogating the Wnt3a-induced epithelial-mesenchymal transition (EMT) in human RPE cells. Our findings suggest that Wnt5a suppresses the pathogenic effects of canonical Wnt signaling in human RPE cells by promoting β-catenin phosphorylation and degradation. Therefore, Wnt5a has significant therapeutic potential for the treatment of AMD. [BMB Reports 2015; 48(9): 525-530]

• 대한안과학회지
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• 제59권12호
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• pp.1152-1159
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• 2018

목적: 중기 나이관련황반변성 환자에서 항산화영양제 복용 후 3년간의 경과 변화를 전향적으로 분석하였다. 대상과 방법: 전향적, 다기관 연구로서 중기 나이관련황반변성으로 진단받은 55명 79안을 대상으로 루테인과 지아잔틴을 복용하게 한 후 전향적으로 관찰하였다. 첫 방문 후 12개월 간격으로 총 36개월간 대비감도검사를 시행하였고, 교정시력 및 중심와 망막두께, 드루젠 부피를 측정하였다. 중심와 망막두께 및 드루젠 부피는 스펙트럼영역 빛간섭단층촬영기를 이용해 측정하였다. 결과: 대상 환자의 임상 양상을 분석한 결과, 환자들의 평균 연령은 $72.46{\pm}7.16$세였다. 대비감도 검사 결과는 종료 시점에서 최초 시점과 비교하여 호전된 양상을 보였고, 특히 3, 6 cycles per degree에서 통계적으로 유의한 차이를 보였다. 최초 환자들의 교정시력은 $0.13{\pm}0.14logMAR$로, 이후 36개월간 유의한 차이가 없었다. 관찰 기간 동안 중심와 망막두께, 드루젠 부피 또한 통계적으로 의미 있는 변화가 없었다. 결론: 중기 나이관련황반변성 환자에서 항산화영양제 복용 후 장기간의 추적관찰 기간 동안 대비감도가 호전되어 시기능 향상에 도움이 되었으며, 교정시력과 중심와 망막두께, 드루젠 부피에는 의미 있는 변화는 없었다. 따라서 항산화영양제의 섭취를 통해 황반 변성의 진행을 감소시키고 시기능의 질적 향상을 기대해 볼 수 있다.

• Molecules and Cells
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• 제43권7호
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• pp.632-644
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• 2020

The molecular mechanism underlying autophagy impairment in the retinal pigment epithelium (RPE) in dry age-related macular degeneration (AMD) is not yet clear. Based on the causative role of poly(ADP-ribose) polymerase 1 (PARP1) in RPE necrosis, this study examined whether PARP1 is involved in the autophagy impairment observed during dry AMD pathogenesis. We found that autophagy was downregulated following H₂O₂-induced PARP1 activation in ARPE-19 cells and olaparib, PARP1 inhibitor, preserved the autophagy process upon H₂O₂ exposure in ARPE-19 cells. These findings imply that PARP1 participates in the autophagy impairment upon oxidative stress in ARPE-19 cells. Furthermore, PARP1 inhibited autolysosome formation but did not affect autophagosome formation in H₂O₂-exposed ARPE-19 cells, demonstrating that PARP1 is responsible for impairment of late-stage autophagy in particular. Because PARP1 consumes NAD⁺ while exerting its catalytic activity, we investigated whether PARP1 impedes autophagy mediated by sirtuin1 (SIRT1), which uses NAD⁺ as its cofactor. A NAD⁺ precursor restored autophagy and protected mitochondria in ARPE-19 cells by preserving SIRT1 activity upon H₂O₂. Moreover, olaparib failed to restore autophagy in SIRT1-depleted ARPE-19 cells, indicating that PARP1 inhibits autophagy through SIRT1 inhibition. Next, we further examined whether PARP1-induced autophagy impairment occurs in the retinas of dry AMD model mice. Histological analyses revealed that olaparib treatment protected mouse retinas against sodium iodate (SI) insult, but not in retinas cotreated with SI and wortmannin, an autophagy inhibitor. Collectively, our data demonstrate that PARP1-dependent inhibition of SIRT1 activity impedes autophagic survival of RPE cells, leading to retinal degeneration during dry AMD pathogenesis.