Age-related macular degeneration (AMD) is central vision loss with aging, was the fourth main cause of blindness in 2015, and has many risk factors, such as cataract surgery, cigarette smoking, family history, hypertension, obesity, long-term smart device usage, etc. AMD is classified into three categories: normal AMD, early AMD, and late AMD, based on angiogenesis in the retina, and can be determined by bis-retinoid N-retinyl-N-retinylidene ethanolamine (A2E)-epoxides from the reaction of A2E and blue light. During the reaction of A2E and blue light, reactive oxygen species (ROS) are synthesized, which gather inflammatory factors, induce carbonyl stress, and finally stimulate the death of retinal pigment epitheliums (RPEs). There are several medications for AMD, such as device-based therapy, anti-inflammatory drugs, anti-VEGFs, and natural products. For device-based therapy, two methods are used: prophylactic laser therapy (photocoagulation laser therapy) and photodynamic therapy. Anti-inflammatory drugs consist of corticosteroids and non-steroidal anti-inflammatory drugs (NSAIDs). Anti-VEGFs are classified antibodies for VEGF, aptamer, soluble receptor, VEGF receptor-1 and -2 antibody, and VEGF receptor tyrosine kinase inhibitor. Finally, additional AMD drug candidates are derived from natural products. For each medication, there are several and severe adverse effects, but natural products have a potency as AMD drugs, as they have been used as culinary materials and/or traditional medicines for a long time. Their major application route is oral administration, and they can be combined with device-based therapy, anti-inflammatory drugs, and anti-VEGFs. In general, AMD drug candidates from natural products are more effective at treating early and intermediate AMD. However, further study is needed to evaluate their efficacy and to investigate their therapeutic mechanisms.

Age-related macular degeneration (AMD) is related to central visual loss in elderly people and, based on the increment in the percentage of the aging population, the number of people suffering from AMD could increase. AMD is initiated by retinal pigment epithelium (RPE) cell death, finally leading to neovascularization in the macula lutea. AMD is an uncurable disease, but the symptom can be suppressed. The current therapy of AMD can be classified into four types: device-based treatment, anti-inflammatory drug treatment, anti-vascular endothelial growth factor treatment, and natural product treatment. All these therapies have adverse effects, however early AMD therapy used with products has several advantages, as it can prevent RPE cell apoptosis in safe doses. Cell death (apoptosis) is caused by various factors, such as oxidative stress, inflammation, carbonyl stress, and a deficiency in essential components for cells, and RPE cell death is related to oxidative stress, inflammation, and carbonyl stress. Some natural products have anti-oxidative effects, anti-inflammation effects, and/or anti-carbonylation effects. The AMD preventive mechanism of natural products varies, with some natural products activating one or more anti-apoptotic pathways, such as the Nrf2/HO-1 anti-oxidative pathway, the anti-inflammasome pathway, and the anti-carbonyl pathway. As AMD drug candidates from natural products effectively inhibit RPE cell death, they have the potential to be developed as drugs for preventing early (dry) AMD.

Age-related macular degeneration (AMD) is one of the leading causes of blindness. AMD is currently incurable; the best solution is to prevent its occurrence. To develop drugs for AMD, it is crucial to have a model system that mimics the symptoms and mechanisms in patients. It is most important to develop safer and more effective anti-AMD drug. In this study, the dose of A2E and the intensity of blue light were evaluated to establish an appropriate atrophic in vitro model of AMD and anti-AMD effect and therapeutic mechanism of Codonopsis lanceolata. The experimental groups included a control group an AMD group treated with A2E and blue light, a lutein group treated with 25 μM lutein after AMD induction, and three groups treated with different doses of C. lanceolata (10, 20, and 50 μg/mL) after AMD induction. Intrinsic apoptotic pathway (Bcl-2 family), anti-oxidative system (Keap1/Nrf2/HO-1 antioxidant response element), and anti-carbonyl effect (4-hydroxynonenal [4-HNE]) were evaluated using immunofluorescence, MTT, TUNEL, FACS, and western blotting analyses. A2E accumulation in the cytoplasm of ARPE-19 cells depending on the dose of A2E. Cell viability of ARPE-19 cells according to the dose of A2E and/or blue light intensity. The population of apoptotic or necrotic cells increased based on the A2E dose and blue light intensity. Codonopsis lanceolata dose-dependently prevented cell death which was induced by A2E and blue light. The antiapoptotic effect of that was caused by activating Keap1/Nrf2/HO-1 pathway, suppressing 4-HNE, and modulating Bcl-2 family proteins like increase of antiapoptotic proteins such as Bcl-2 and Bcl-XL and decrease of proapoptotic protein such as Bim. Based on these findings, 30 μM A2E and 20 mW/cm² blue light on adult retinal pigment epithelium-19 cells was an appropriate condition for AMD model and C. lanceolata shows promise as an anti-AMD agent.

Objective: To evaluate the therapeutic efficacy and inflammatory modulatory effects of combined 0.01% atropine eye drops and orthokeratology (OK) lenses in controlling myopia progression among adolescent patients. Methods: This retrospective study analyzed clinical data from 90 adolescent patients (90 eyes) with myopia treated from April 2021 to June 2023. Patients were divided into two groups: control group (n=45, treated with OK lenses alone) and observation group (n=45, treated with OK lenses combined with 0.01% atropine). Baseline and 1-year post-treatment measurements included refractive status, axial length (AL), corneal parameters, ocular surface indices, tear film stability, endothelial cell morphology, inflammatory cytokine levels in tears, and incidence of adverse events. Results: After 1 year, both groups showed myopic progression, but the observation group exhibited significantly less axial elongation (0.12 ± 0.08 mm vs 0.21 ± 0.09 mm; p < 0.001) and smaller increases in refractive error (p < 0.001). Corneal curvature and central corneal thickness were also significantly lower in the observation group (p < 0.05). The pupil diameter increased more in the observation group (p = 0.002), consistent with atropine’s pharmacologic effect. Ocular surface damage was less severe, with lower OSDI (p = 0.002) and staining scores (p < 0.001). Tear film stability was better preserved, as reflected by higher NIBUT and TBUT values (p < 0.05). No significant differences in endothelial cell density or hexagonality were observed (p > 0.6). Tear cytokine levels (IL-1β, IL-6, TNF-α) increased in both groups but were significantly lower in the observation group (all p < 0.01). The incidence of adverse reactions was low and comparable between groups (p = 0.235), with no severe events reported. Conclusion: The combination of 0.01% atropine eye drops with orthokeratology lenses is more effective than orthokeratology alone in controlling myopia progression and mitigating ocular surface inflammation in adolescents, without increasing adverse effects.

Myopia is a major global public health concern, with a particularly high and increasing prevalence in East Asia. Although significant progress has been made in regard to developing strategies to slow the progression of myopia, the precise biological mechanisms underlying the onset and progression of myopia remain unclear. Repeated low-level red light (RLRL) therapy, a novel non-invasive photobiomodulation (PBM) technique, has demonstrated promising efficacy for controlling axial elongation and refractive error progression. This review first outlines the clinical definition, epidemiology, and global health impact of myopia, followed by the etiology-based pathogenesis and corresponding intervention strategies. Special attention has been given to emerging mechanistic evidence supporting RLRL, particularly its role in activating mitochondrial cytochrome c oxidase (CCO), enhancing retinal metabolism, influencing choroidal changes in blood perfusion and thickness, and in scleral remodeling. Finally, the feasibility and potential mechanism of the RLRL therapy for slowing myopia progression have been discussed from the perspective of safety.