Dim light at night shifts microglia to a pro-inflammatory state after cerebral ischemia, altering stroke outcome in mice.

Circadian rhythms are endogenous biological cycles that regulate physiology and behavior and are set to precisely 24-h by light exposure. Light at night (LAN) dysregulates physiology and function including immune response; a critical component that contributes to stroke pathophysiological progression of neuronal injury and may impair recovery from injury. The goal of this study is to explore the effects of dim LAN (dLAN) in a murine model of ischemic stroke to assess how nighttime lighting from hospital settings can affect stroke outcome. Further, this study sought to identify mechanisms underlying pathophysiological changes to immune response after circadian disruption. Male and female adult Swiss Webster (CFW) mice were subjected to transient or permanent focal cerebral ischemia, then were subsequently placed into either dark night conditions (LD) or one night of dLAN (5 lx). 24 h post-stroke, sensorimotor impairments and infarct sizes were quantified. A single night of dLAN following MCAO increased infarct size and sensorimotor deficits across both sexes and reduced survival in males after 24 h. Flow cytometry was performed to assess microglial phenotypes after MCAO, and revealed that dLAN altered the percentage of microglia that express pro-inflammatory markers (MHC II+ and IL-6) and microglia that express CD206 and IL-10 that likely contributed to poor ischemic outcomes. Following these results, microglia were reduced in the brain using Plexxikon 5622 (PLX 5622) a CSFR1 inhibitor, then the mice received an MCAO and were exposed to LD or dLAN conditions for 24 h. Microglial depletion by PLX5622 resulted in infarct sizes that were comparable between lighting conditions. This study provides supporting evidence that environmental lighting exacerbates ischemic injury and post-stroke mortality by a biological mechanism that exposure to dLAN causes a fundamental shift of activated microglial phenotypes from beneficial to detrimental at an early time point after stroke, resulting in irreversible neuronal death.

Phototoxicity avoidance is a potential therapeutic approach for retinal dystrophy caused by EYS dysfunction.

Inherited retinal dystrophies (IRDs) are progressive diseases leading to vision loss. Mutation in the eyes shut homolog (EYS) gene is one of the most frequent causes of IRD. However, the mechanism of photoreceptor cell degeneration by mutant EYS has not been fully elucidated. Here, we generated retinal organoids from induced pluripotent stem cells (iPSCs) derived from patients with EYS-associated retinal dystrophy (EYS-RD). In photoreceptor cells of RD organoids, both EYS and G protein-coupled receptor kinase 7 (GRK7), one of the proteins handling phototoxicity, were not in the outer segment, where they are physiologically present. Furthermore, photoreceptor cells in RD organoids were vulnerable to light stimuli, and especially to blue light. Mislocalization of GRK7, which was also observed in eys-knockout zebrafish, was reversed by delivering control EYS into photoreceptor cells of RD organoids. These findings suggest that avoiding phototoxicity would be a potential therapeutic approach for EYS-RD.

Sensitivity to light in bipolar disorder: implications for research and clinical practice.

Circadian dysfunction is a core feature of bipolar disorder and may be due, at least in part, to abnormalities of non-visual photoreception. We critically review the evidence for light hypersensitivity in bipolar disorder and discuss how this may shape future research and clinical innovation, with a focus on a possible novel mechanism of action for lithium.

Dersimelagon in Erythropoietic Protoporphyrias.

BACKGROUND: Erythropoietic protoporphyria and X-linked protoporphyria are inborn errors of heme biosynthesis that cause elevated circulating levels of metal-free protoporphyrin and phototoxicity. Both disorders are characterized by excruciating phototoxic attacks after exposure to visible light. Dersimelagon is a new, orally administered, selective melanocortin 1 receptor agonist that increases levels of skin eumelanin. METHODS: We conducted a randomized, placebo-controlled, phase 2 trial to investigate the efficacy and safety of dersimelagon with respect to the time to onset and the severity of symptoms associated with sunlight exposure in patients with erythropoietic protoporphyria or X-linked protoporphyria. Patients 18 to 75 years of age were randomly assigned in a 1:1:1 ratio to receive placebo or dersimelagon at a dose of 100 or 300 mg once daily for 16 weeks. The primary end point was the change from baseline to week 16 in the time to the first prodromal symptom associated with sunlight exposure. Patients recorded daily sunlight exposure and symptom data in an electronic diary. Quality of life and safety were also assessed. RESULTS: Of the 102 patients (93 with erythropoietic protoporphyria and 9 with X-linked protoporphyria) who underwent randomization, 90% completed the treatment period. The mean daily time to the first prodromal symptom associated with sunlight exposure increased significantly with dersimelagon: the least-squares mean difference from placebo in the change from baseline to week 16 was 53.8 minutes in the 100-mg dersimelagon group (P = 0.008) and 62.5 minutes in the 300-mg dersimelagon group (P = 0.003). The results also suggest that quality of life improved in patients receiving dersimelagon as compared with placebo. The most common adverse events that occurred or worsened during treatment were nausea, freckles, headache, and skin hyperpigmentation. CONCLUSIONS: At both doses evaluated, dersimelagon significantly increased the duration of symptom-free sunlight exposure in patients with erythropoietic protoporphyria or X-linked protoporphyria. (Funded by Mitsubishi Tanabe Pharma; Endeavor ClinicalTrials.gov number, NCT03520036.).

Sex- and age-specific association between outdoor light at night and obesity in Chinese adults: A national cross-sectional study of 98,658 participants from 162 study sites.

Background: Exposure to light at night (LAN) is a potent disruptor of the circadian system. Whether LAN exposure exerts a sex- or age-specific influence on obesity needs investigation. Objectives: To estimate the sex- and age-specific associations of exposure to outdoor LAN and obesity based on a national and cross-sectional survey. Methods: The study included a nationally representative sample of 98,658 adults aged ≥ 18 years who had lived in their current residence for ≥ 6 months from 162 study sites across mainland China in 2010. Outdoor LAN exposure was estimated from satellite imaging data. General obesity was defined as body-mass index (BMI) ≥ 28 kg/m2 and central obesity was defined as waist circumference ≥ 90 cm in men and ≥ 85 cm in women. Linear and logistic regression models were used to examine the associations between LAN exposure and prevalent obesity in sex and age categories. Results: A monotonically increasing association of outdoor LAN with BMI, waist circumference was observed in all sex and age categories, except for adults aged 18-39 years. Significant associations of LAN exposure with prevalent obesity were observed in each sex and age category, especially in men and older people. Per 1-quintile increase in LAN was associated with 14% increased odds of general obesity in men (odds ratio, OR=1.14, 95% confidence interval, CI=1.07-1.23) and 24% in adults aged ≥ 60 years (OR=1.24, 95% CI=1.14-1.35). Per 1-quintile increase in LAN was associated with 19% increased odds of central obesity in men (OR=1.19, 95% CI=1.11-1.26) and 26% in adults aged ≥ 60 years (OR=1.26, 95% CI=1.17-1.35). Conclusions: Increased chronic outdoor LAN exposure was associated with increased prevalence of obesity in sex- and age- specific Chinese populations. Public health policies on reducing light pollution at night might be considered in obesity prevention.

Long-term Pu-erh tea consumption improves blue light-induced depression-like behaviors.

Blue light emitted by smartphones and tablets at night increases the risk of depression. Pu-erh tea has been reported to reduce the risk of depression by regulating tryptophan metabolism, but its underlying protective mechanism on depression induced by blue light at night (BLAN) remains unclear. In this work, two groups of C57BL6/J mice were given water or 0.25% (w/v) Pu-erh tea for 120 days, followed by a 45-day BLAN treatment (400 lux blue light between 21:00 and 23:00) to simulate blue light emitted from electronic equipment. Our results indicated that BLAN induced depression-like behaviors and gut microbiota disorders in healthy mice. Pu-erh tea intake significantly reshaped the gut microbiome (especially Bifidobacterium) and regulated the metabolism of short-chain fatty acids (SCFAs) which protected the integrity of the intestinal barrier. This improvement further reduced blood-brain barrier (BBB) damage and alleviated neuroinflammation by inhibiting MyD88/NF-κB pathways which finally regulated neurotransmitters such as brain-derived neurotrophic factor (BDNF) and serotonin (5-hydroxytryptamine, 5-HT). Collectively, 0.25% (w/v) Pu-erh tea has the potential to prevent BLAN-induced depression-like behaviors by reshaping the gut microbiota and increasing the generation of SCFAs via the gut-brain axis.

Ação da luz visível na oxidação da melanina e no descolorimento do cabelo / Action of the visible on the melanin oxidation and hair discoloration

O dano capilar causado pelo descolorimento oxidativo é muito intenso, sendo que dois fatores são responsáveis por essa ação: primeiro, a ação direta e danosa do oxidante em diversas estruturas capilares e segundo, o dano oxidativo primário facilita o dano causado por outros agentes físicos (luz, temperatura) e químicos (tensoativos), que comumente tem ação nos cabelos. Desenvolver conceitos e tecnologias que possam tornar o oxidante específico para a melanina e por conseguinte efetuando o descolorimento sem causar danos ao fio é extremamente desejável. Neste trabalho buscaremos entender de que forma a luz visível pode aumentar a ação do oxidante sem danificar o fio colateralmente. O objetivo principal deste trabalho é demonstrar que é possível utilizar a luz visível, que é absorvida pela melanina, para tornar esse pigmento mais suscetível ao agente oxidante e desta forma, permitir que o descolorimento seja realizado com concentrações pequenas de oxidante. Também almejamos desenvolver métodos de análises por microscopia ótica de fluorescência e de reflexão para mensurar o dano nas estruturas dos fios processados com oxidante e na presença ou ausência da luz

The capillary damage caused by oxidative discoloration is very intense, and two factors are responsible for this action: first, the direct and harmful action of the oxidant on several capillary structures and second, the primary oxidative damage facilitates the damage caused by other physical agents (light, temperature) and chemicals (surfactants), which commonly have action on the hair. Developing concepts and technologies that can make the oxidant specific to melanin and therefore discoloring without causing damage to the hair is extremely desirable. In this work we will try to understand how visible light can increase the oxidant's action without damaging the wire collaterally. The main objective of this work is to demonstrate that it is possible to use visible light, which is absorbed by melanin, to make this pigment more susceptible to the oxidizing agent and, thus, to allow the discoloration to be carried out with small concentrations of oxidizer. We also aim to develop methods of analysis by optical fluorescence and reflection microscopy to measure the damage to the structures of the threads processed with oxidizer and in the presence or absence of light

Effects of light wavelength exposure during in vitro blastocyst production on preimplantation development of mouse embryos.

CONTEXT: Despite the absence of light within the body, the application of microscopy during stages of in vitro embryo production has led to the discovery of light irradiation effects on embryo preimplantation development. AIMS: To determine the optimal light irradiation wavelengths at various embryo stages for improving the preimplantation development of mouse embryos and the quality (total cell number) of blastocysts. METHOD: All in vitro procedures of zygote or 2-cell embryo manipulation, embryo monitoring, and culture medium exchange were conducted under visible (390-750nm), blue (445-500nm), green (500-575nm), yellow (575-585nm), or red (620-750nm) light irradiation wavelength. KEY RESULTS: We found that blue, green, and yellow light irradiation during in vitro blastocyst production from zygotes significantly improved blastocyst production and quality, compared to visible and red light irradiation. However, 2-cell embryos exposed to yellow light during in vitro blastocyst production produced significantly more high-quality blastocysts than did 2-cell embryos exposed to visible, blue, green, or red light. After exposure to blue and green - but not yellow - light during in vitro zygote manipulation, yellow light irradiation during embryo monitoring and culture medium exchange triggered significant retardation of preimplantation development. CONCLUSION: These results demonstrate that yellow light irradiation during in vitro blastocyst production, regardless of embryo stage, improves preimplantation development of mouse embryos. IMPLICATIONS: The present study will contribute to produce greater high-quality blastocysts and reduce experimental errors generated by light exposure during mouse embryo-related studies.

The effect of a chrysanthemum water extract in protecting the retina of mice from light damage.

BACKGROUND: Oxidative stress can induce age-related diseases. Age-related retinal diseases, such as age-related macular degeneration (AMD), are difficult to cure owing to their complicated mechanisms. Although anti-neovascular therapeutics are used to treat wet AMD, vision cannot always be completely restored, and disease progression cannot always be inhibited. Therefore, determining a method to prevent or slow retinal damage is important. This study aimed to investigate the protective effect of a chrysanthemum water extract rich in flavone on the oxidatively stressed retina of mice. METHODS: Light damage was induced to establish oxidative stress mouse models. For in vitro experiments, ARPE-19 cells were cultured and divided into four groups: control, light-damaged, and low- and high-dose chrysanthemum extract. No treatment was administered in the control group. The light-damaged and low- and high-dose chrysanthemum extract groups were exposed to a similar white light level. The chrysanthemum extract was added at a low dose of 0.4 mg/mL or a high dose of 1.0 mg/mL before cell exposure to 2500-lx white light. Reactive oxygen species (ROS) level and cellular viability were measured using MTT and immunofluorescence staining. For in vivo experiments, C57BL/6 J mice were divided into the same four groups. Low- (0.23 g/kg/day) and high-dose (0.38 g/kg/day) chrysanthemum extracts were continuously intragastrically administered for 8 weeks before mouse exposure to 10,000-lx white light. Retinal function was evaluated using electroretinography. In vivo optical coherence tomography and in vitro haematoxylin and eosin staining were performed to observe the pathological retinal changes in each group after light damage. Fluorescein fundus angiography of the arteriovenous vessel was performed, and the findings were analysed using the AngioTool software. TUNEL immunofluorescence staining was used to assess isolated retinal apoptosis. RESULTS: In vitro, increased ROS production and decreased ARPE-19 cell viability were found in the light-damaged group. Improved ARPE-19 cell viability and reduced ROS levels were observed in the chrysanthemum extract treatment groups. In vivo, dysfunctional retinas and abnormal retinal structures were found in the light-damaged group, as well as increased apoptosis in the retinal ganglion cells (RGCs) and inner and outer nuclear layers. The apoptosis rate in the same layers was lower in the chrysanthemum extract treatment groups than in the light-damaged group. The production of antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), increased in the treatment groups. NF-κB in the nucleus and TNF-α were more highly expressed in the light-damaged group than in the low- and high-dose chrysanthemum extract groups. CONCLUSIONS: Light damage-induced retinal oxidative stress can lead to ROS accumulation in the retinal tissues. Herein, RGC and photoreceptor layer apoptosis was triggered, and NF-κB in the nucleus and TNF-α were highly expressed in the light-damaged group. Preventive chrysanthemum extract administration decreased ROS production by increasing SOD, CAT, and GSH-Px activities and reversing the negative changes, demonstrating a potential protective effect on the retina.

Exposure to b-LED Light While Exerting Antimicrobial Activity on Gram-Negative and -Positive Bacteria Promotes Transient EMT-like Changes and Growth Arrest in Keratinocytes.

While blue LED (b-LED) light is increasingly being studied for its cytotoxic activity towards bacteria in therapy of skin-related infections, its effects on eukaryotic cells plasticity are less well characterized. Moreover, since different protocols are often used, comparing the effect of b-LED towards both microorganisms and epithelial surfaces may be difficult. The aim of this study was to analyze, in the same experimental setting, both the bactericidal activity and the effects on human keratinocytes. Exposure to b-LED induced an intense cytocidal activity against Gram-positive (i.e, Staphylococcus aureus) and Gram-negative (i.e., Pseudomonas aeruginosa) bacteria associated with catheter-related infections. Treatment with b-LED of a human keratinocyte cell line induced a transient cell cycle arrest. At the molecular level, exposure to b-LED induced a transient downregulation of Cyclin D1 and an upregulation of p21, but not signs of apoptosis. Interestingly, a transient induction of phosphor-histone γ-H2Ax, which is associated with genotoxic damages, was observed. At the same time, keratinocytes underwent a transient epithelial to mesenchymal transition (EMT)-like phenotype, characterized by E-cadherin downregulation and SNAIL/SLUG induction. As a functional readout of EMT induction, a scratch assay was performed. Surprisingly, b-LED treatment provoked a delay in the scratch closure. In conclusion, we demonstrated that b-LED microbicidal activity is associated with complex responses in keratinocytes that certainly deserve further analysis.

Topological Relationships Cytoskeleton-Membrane Nanosurface-Morphology as a Basic Mechanism of Total Disorders of RBC Structures.

The state of red blood cells (RBCs) and their functional possibilities depend on the structural organization of the membranes. Cell morphology and membrane nanostructure are compositionally and functionally related to the cytoskeleton network. In this work, the influence of agents (hemin, endogenous oxidation during storage of packed RBCs, ultraviolet (UV) radiation, temperature, and potential of hydrogen (pH) changes) on the relationships between cytoskeleton destruction, membrane nanostructure, and RBC morphology was observed by atomic force microscope. It was shown that the influence of factors of a physical and biochemical nature causes structural rearrangements in RBCs at all levels of organization, forming a unified mechanism of disturbances in relationships "cytoskeleton-membrane nanosurface-cell morphology". Filament ruptures and, consequently, large cytoskeleton pores appeared. The pores caused membrane topological defects in the form of separate grain domains. Increasing loading doses led to an increase in the number of large cytoskeleton pores and defects and their fusion at the membrane nanosurfaces. This caused the changes in RBC morphology. Our results can be used in molecular cell biology, membrane biophysics, and in fundamental and practical medicine.

A randomized controlled trial on the effects of blue-blocking glasses compared to partial blue-blockers on sleep outcomes in the third trimester of pregnancy.

OBJECTIVE: Sleep disturbances are common in pregnancy. Blocking blue light has been shown to improve sleep and may be a suitable intervention for sleep problems during pregnancy. The present study investigated the effects of blue light blocking in the evening and during nocturnal awakenings among pregnant women on primary sleep outcomes in terms of total sleep time, sleep efficiency and mid-point of sleep. METHODS: In a double-blind randomized controlled trial, 60 healthy nulliparous pregnant women in the beginning of the third trimester were included. They were randomized, using a random number generator, either to a blue-blocking glass intervention (n = 30) or to a control glass condition constituting partial blue-blocking effect (n = 30). Baseline data were recorded for one week and outcomes were recorded in the last of two intervention/control weeks. Sleep was measured by actigraphy, sleep diaries, the Bergen Insomnia Scale, the Karolinska Sleepiness Scale and the Pre-Sleep Arousal Scale. RESULTS: The results on the primary outcomes showed no significant mean difference between the groups at posttreatment, neither when assessed with sleep diary; total sleep time (difference = .78[min], 95%CI = -19.7, 21.3), midpoint of sleep (difference = -8.9[min], 95%CI = -23.7, 5.9), sleep efficiency (difference = -.06[%], 95%CI = -1.9, 1.8) and daytime functioning (difference = -.05[score points], 95%CI = -.33, .22), nor by actigraphy; total sleep time (difference = 13.0[min], 95%CI = -9.5, 35.5), midpoint of sleep (difference = 2.1[min], 95%CI = -11.6, 15.8) and sleep efficiency (difference = 1.7[%], 95%CI = -.4, 3.7). On the secondary outcomes, the Bergen Insomnia Scale, the Karolinska Sleepiness Scale and the Pre-Sleep Arousal Scale the blue-blocking glasses no statistically significant difference between the groups were found. Transient side-effects were reported in both groups (n = 3). CONCLUSIONS: The use of blue-blocking glasses compared to partially blue-blocking glasses in a group of healthy pregnant participants did not show statistically significant effects on sleep outcomes. Research on the effects of blue-blocking glasses for pregnant women with sleep-problems or circadian disturbances is warranted. TRIAL REGISTRATION: The trial is registered at ClinicalTrials.gov (NCT03114072).

The roles of mitochondrial dynamics and NLRP3 inflammasomes in the pathogenesis of retinal light damage.

With the widespread popularity of electronic products and the diversification of lighting equipment, ocular photochemical damage caused by light has attracted research attention. Although such equipment mainly cause damage to the retina, the specific pathogenesis has not been systematically elucidated. Thus, the goal of this study was to explore the relationship between mitochondrial dysfunction and the activation of the NOD-like receptor protein 3 (NLRP3) inflammasome in retinal cell death caused by light damage. We used a white light-emitting diode source to establish a mouse model of retinal light damage and observed significant changes of retinal structure and an impairment of visual function. Further experiments revealed that dynamin-related protein 1 (Drp1)-mediated excessive mitochondrial fission induced overproduction of reactive oxygen species in the retinal cells, leading to apoptosis, activation of microglia, and formation of the NLRP3 inflammasome. This, in turn, triggered a series of inflammatory cascade reactions, leading to pyroptosis. We also carried out red light and Drp1 inhibitor treatment and found that retinal damage and the decline in visual function caused by white light could be partially ameliorated. In conclusion, this study clarified the association between mitochondrial dynamics and the NLRP3 inflammasome in retinal light damage and provides opportunities for therapeutic intervention.

High-Light-Induced Stress Activates Lipid Deacylation at the Sn-2 Position in the Cyanobacterium Synechocystis Sp. PCC 6803.

Cyanobacterial mutants defective in acyl-acyl carrier protein synthetase (Aas) produce free fatty acids (FFAs) because the FFAs generated by deacylation of membrane lipids cannot be recycled. An engineered Aas-deficient mutant of Synechocystis sp. PCC 6803 grew normally under low-light (LL) conditions (50 µmol photons m-2 s-1) but was unable to sustain growth under high-light (HL) conditions (400 µmol photons m-2 s-1), revealing a crucial role of Aas in survival under the HL conditions. Several-times larger amounts of FFAs were produced by HL-exposed cultures than LL-grown cultures. Palmitic acid accounted for ∼85% of total FFAs in HL-exposed cultures, while C18 fatty acids (FAs) constituted ∼80% of the FFAs in LL-grown cultures. Since C16 FAs are esterified to the sn-2 position of lipids in the Synechocystis species, it was deduced that HL irradiation activated deacylation of lipids at the sn-2 position. Heterologous expression of FarB, the FFA exporter protein of Neisseria lactamica, prevented intracellular FFA accumulation and rescued the growth defect of the mutant under HL, indicating that intracellular FFA was the cause of growth inhibition. FarB expression also decreased the 'per-cell' yield of FFA under HL by 90% and decreased the proportion of palmitic acid to ∼15% of total FFA. These results indicated that the HL-induced lipid deacylation is triggered not by strong light per se but by HL-induced damage to the cells. It was deduced that there is a positive feedback loop between HL-induced damage and lipid deacylation, which is lethal unless FFA accumulation is prevented by Aas.

Digital asthenopia: blue-blocking lenses and + 0,40D additional power in the near zone, for eye strain, accommodation and convergence functions / Astenopia digital: avaliação de lentes com filtro de luz azul e poder adicional de +0,40D na zona de perto, para fadiga visual e nas funções de convergência e acomodação

ABSTRACT Purpose Evaluate blue-violet light filter and additional power of +0.40 D in the near zone ophthalmic lenses, on convergence, accommodative functions, and symptoms of digital asthenopia (DA). Methods Randomized study in cross-over design conducted on 49 volunteers (age, 29 ± 5.5 years; male: female, 18:31). Each subject wore test (+0.40 D in the near zone) and control lenses (regular single vision) for 4 weeks in randomized order. Both lenses had a selective blue-violet light filter. A baseline measurement was taken with the subjects' current updated glasses. Accommodation amplitude (AA) and near point of convergence (NPC) were measured binocularly with the RAF ruler. DA was evaluated by a questionnaire. Results No significant difference (p=.52) was found for AA comparing baseline (11.50±1.88 D), test (11.61± 1.62 D), and control SV lenses (11.88±1.50 D). No significant difference was found for NPC (p=.94), between baseline (6.50 ± 2.89cm), test (6.71± 3.49) and control SV lenses (6.82± 3.50 cm). No significant difference was found comparing test and control SV lenses in symptoms of DA (p=0.20). Conclusions The +0.40 D lenses have no negative impact on convergence or loss of accommodation power. The +0.40 D and control SV lenses had a similar impact on attenuating symptoms of DA.

RESUMO Objetivo Avaliar os efeitos do uso de lentes oftálmicas com filtro seletivo de luz azul-violeta, sem e com poder adicional de + 0,4D na zona de perto nas funções de acomodação e convergência e para sintomas de astenopia digital (AD). Métodos Ensaio clínico controlado, randomizado e mascarado, com 49 voluntários (idade, 29 ± 5,5 anos; masculino: feminino, 18: 31). Cada participante usou lentes de teste (+0,40 D na zona de perto) e controle (visão simples), por 4 semanas de forma randomizada. Ambas as lentes tinham filtro seletivo de luz azul-violeta. A medição inicial (baseline) foi feita com os óculos atualizados de cada participante. A amplitude de acomodação (AA) e o ponto de convergência próximo (PPC) foram medidos binocularmente com a régua RAF. A AD foi avaliada por um questionário. Resultados Não houve diferença estatisticamente significante (p=0,52) para as medidas de AA comparando as lentes baseline (11,50±1,88 D), teste (11,61±1,62 D) e controle VS (11,88±1,50 D). Nenhuma diferença significativa foi encontrada para a medida do PPC (p=0,94), entre as lentes baseline (6,50 ± 2,89cm), teste (6,71±3,49) e controle VS (6,82±3,50 cm). Nenhuma diferença significativa foi encontrada comparando lentes teste de VS e controle nos sintomas de AD (p=0,20). Conclusões As lentes com +0,40 D não têm impacto negativo na convergência ou na perda de acomodação. As lentes +0,40 D e controle VS, tiveram impacto semelhante na redução dos sintomas de AD.

Lotus Seedpod Proanthocyanidins Protect Against Light-Induced Retinal Damage via Antioxidative Stress, Anti-Apoptosis, and Neuroprotective Effects.

BACKGROUND Over-exposure to visible white light can cause retinal damage. Lotus seedpod proanthocyanidins (LSPCs) possess a variety of biological activities, including potent antioxidant and protective effects. Herein, this study observed whether LSPCs can protect against light exposure-induced retinal damage. MATERIAL AND METHODS We randomly separated 40 Prague-Dawley rats into a control group, a light exposure-induced retinal injury model group, and low-dose (50 mg/kg), medium-dose (100 mg/kg), and high-dose (100 mg/kg) LSPCs groups. Light-induced retinal damage models were established by 5000±200 Lx light treatment for 6 h. Five days and 0.5 h before the light treatment, rats in the LSPCs groups were separately administered 50, 100, and 200 mg/kg LSPCs by gavage. After 7 days, H&E staining of retinal sections was performed and the thickness of the ONL was measured. Oxidative stress-related markers and antioxidant enzymes were measured in serum by biochemical testing. TUNEL staining of retinal sections was also performed. Apoptosis-relevant proteins were examined by RT-qPCR and western blotting. GFAP expression was examined with immunohistochemistry. RESULTS Our H&E staining showed that LSPCs can prevent retinal degeneration following light exposure. Histological analysis showed a significant reduction in the ONL thickness of light exposure-induced retinal injury rats, but LSPCs substantially improved the ONL thickness. LSPCs markedly ameliorated the light-induced increase in levels of MDA, NO, and NOS, and decrease in activity of GSH-Px and SOD. Moreover, LSPCs treatment alleviated light-induced retinal apoptosis and limited the light-induced increase in GFAP expression. CONCLUSIONS LSPCs effectively attenuated light-induced retinal damage through antioxidative stress, anti-apoptosis, and neuroprotective effects.